title: Mint-ChIP-seq from neural progenitor cell (ENCSR069EIG)

summary:
H3K36me3 Mint-ChIP-seq on human H9 derived neural progenitor cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: total RNA-seq from macrophage (ENCSR171WZJ)

status: Public on Jun 15 2021

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Expression profiling by high throughput sequencing

summary:
Ribo depletion RNA-seq on chromatin fraction RNA which is part of BMDM cell pre-treated with 100 ng/ml Lipid A 12 hours, washed out for 12 hours, and stimulated with 100 ng/ml Lipid A for 35 minute.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR173THP)

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
H3K9me3 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: WGS from transverse colon (ENCSR246MMZ)

summary:
The data contained in this experiment correspond to Illumina-based whole genome shotgun sequencing of EN-TEX donor ENCDO845WKR, a 37 year old male. There are two libraries: PCR-based (9-cycle, ENCLB436FSE) and PCR-free (ENCLB480CRB), both sequenced on multiple lanes to a combined depth of ~ 60X in PE125 format.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD14-positive monocyte (ENCSR165PMH)

summary:
Control Mint-ChIP-seq on human CD14-positive monocyte

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR158UEK)

summary:
H3K4me3 Mint-ChIP-seq on human CD4-positive, CD25-positive, alpha-beta regulatory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR163WVR)

summary:
H3K9me3 Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive B cell (ENCSR163IRW)

summary:
Control Mint-ChIP-seq of naive B cell originated from naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD14-positive monocyte (ENCSR167XYG)

summary:
H3K9me3 Mint-ChIP-seq on human CD14-positive monocyte

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from immature natural killer cell (ENCSR158VSE)

summary:
H3K36me3 Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from IgD-negative memory B cell (ENCSR157JIS)

summary:
H3K36me3 Mint-ChIP-seq on human IgD-negative memory B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR243QSZ)

summary:
H3K9me3 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR163GRD)

summary:
H3K4me1 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR245HFY)

summary:
H3K27ac ChIP-seq on CD4-positive, alpha-beta memory T cell male adult (43 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR243EIU)

summary:
Control Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR156VQN)

summary:
Control Mint-ChIP-seq on human CD4-positive, CD25-positive, alpha-beta regulatory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from immature natural killer cell (ENCSR169WAD)

summary:
Control Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from immature natural killer cell (ENCSR242ARJ)


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR239OWL)

summary:
H3K36me3 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from immature natural killer cell (ENCSR061ATV)

summary:
H3K9me3 Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from IgD-negative memory B cell (ENCSR238WFK)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from H9 (ENCSR243FOM)

summary:
H3K4me1 Mint-ChIP-seq on human H9

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR242OUP)


title: Mint-ChIP-seq from brain (ENCSR246IBU)

summary:
H3K4me3 Mint-ChIP-seq on human PGP1 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from GM23338 (ENCSR068ZVD)

summary:
H3K4me3 Mint-ChIP-seq on human GM23338

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR058IYH)

summary:
H3K27me3 Mint-ChIP-seq on human CD4-positive, CD25-positive, alpha-beta regulatory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated B cell (ENCSR156BXM)

summary:
H3K4me1 ChIP-seq on B cell male adult (22 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR236SCE)

summary:
H3K36me3 Mint-ChIP-seq on human PGP1 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR151ARX)

summary:
H3K9me3 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR057IZD)

summary:
H3K9me3 Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: WGS from K562 (ENCSR053AXS)

summary:
The data contained in this Experiment come from 10X Chromium Genomics WGS of K562 cell line using the Chromium™ Genome v2 Library Kit & Gel Bead Kit

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from immature natural killer cell (ENCSR056GJY)

summary:
H3K36me3 Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from activated CD4 positive, naive alpha-beta T cell (ENCSR053AWV)

summary:
Control Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (43 years) treated with anti-CD3 and anti-CD28 coated beads

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from immature natural killer cell (ENCSR050UUC)


title: Control ChIP-seq from K562 (ENCSR236QAK)

summary:
ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR052KGC)

summary:
H3K27ac Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR148ICM)


title: WGS from SK-N-MC (ENCSR236KYS)


title: Control Mint-ChIP-seq from B cell (ENCSR051DHR)

summary:
Control Mint-ChIP-seq of B cell male adult (22 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: WGS from K562 (ENCSR045NDZ)


title: Control Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR150CMT)

summary:
Control Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from brain (ENCSR141MUD)

summary:
Control Mint-ChIP-seq on human PGP1 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD4-positive, alpha-beta T cell (ENCSR046DRK)

summary:
H3K27ac Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (20 years) treated with 10 ng

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR232VZV)

summary:
H3K27ac Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (43 years) treated with 10 ng

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR142VGG)

summary:
H3K27ac Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive B cell (ENCSR141MKN)

summary:
H3K27ac Mint-ChIP-seq on human naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR231XAP)

summary:
H3K4me1 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR232JJY)


title: Mint-ChIP-seq from activated CD4 positive, naive alpha-beta T cell (ENCSR227HTN)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR231ZZH)

summary:
H3K4me3 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from T-cell (ENCSR220CDK)

summary:
H3K36me3 ChIP-seq on T-cell male adult (38 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from IgD-negative memory B cell (ENCSR147BRW)


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR043JIA)

summary:
H3K4me1 Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR045KAM)

summary:
H3K9me3 Mint-ChIP-seq on human H9 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR231SVU)

summary:
Control Mint-ChIP-seq of CD8-positive, alpha-beta memory T cell originated from CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR235WEI)

summary:
H3K4me3 Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD4 positive, naive alpha-beta T cell (ENCSR047QYF)


title: Mint-ChIP-seq from immature natural killer cell (ENCSR225GZF)

summary:
H3K27me3 Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR218MSP)

summary:
H3K36me3 Mint-ChIP-seq of CD8-positive, alpha-beta memory T cell male adult (30 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from H9 (ENCSR134OWL)

summary:
H3K9me3 Mint-ChIP-seq on human H9

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR217SHH)


title: Mint-ChIP-seq from neural crest cell (ENCSR133QMT)


title: Mint-ChIP-seq from CD4-positive naive resting alpha-beta T cell (ENCSR217BBP)

summary:
H3K4me1 ChIP-seq on CD4-positive naive resting alpha-beta T cell male adult (43 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR036YVP)

summary:
H3K4me1 Mint-ChIP-seq on human CD4-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR133GLP)

summary:
H3K27me3 Mint-ChIP-seq of CD8-positive, alpha-beta memory T cell male adult (30 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR128KDZ)

summary:
Control Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR034OUM)

summary:
Control Mint-ChIP-seq on human naive thymus-derived CD4-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR035PJY)

summary:
H3K36me3 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR127UUU)

summary:
Control Mint-ChIP-seq on human CD4-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: WGS from K562 (ENCSR025GPQ)

summary:
These data correspond to shotgun PE151 Illumina sequencing done on long insert fragmented gDNA from the K562 cell line

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR217AJC)

summary:
H3K27ac Mint-ChIP-seq on human H9 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR216ZVA)

summary:
H3K27me3 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive B cell (ENCSR030WTO)

summary:
H3K4me1 Mint-ChIP-seq on human naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR123ZAT)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR131ZVC)

summary:
H3K4me3 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from T-cell (ENCSR214UVC)


title: Control Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR128CIX)


title: WGS from T47D (ENCSR121TMQ)


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR122JCM)

summary:
H3K27me3 Mint-ChIP-seq of CD8-positive, alpha-beta memory T cell originated from CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR127HNP)

summary:
H3K27me3 Mint-ChIP-seq on human PGP1 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from astrocyte (ENCSR020LAQ)

summary:
H3K4me3 Mint-ChIP-seq on human PGP1 derived astrocyte

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR034MTZ)

summary:
Control Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta T cell (ENCSR213EES)


title: Mint-ChIP-seq from CD4-positive naive resting alpha-beta T cell (ENCSR019OML)

summary:
H3K4me3 ChIP-seq on CD4-positive naive resting alpha-beta T cell male adult (43 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from GM23338 (ENCSR212MTU)

summary:
H3K4me1 Mint-ChIP-seq on human GM23338

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR019FIH)


title: Mint-ChIP-seq from CD4-positive, alpha-beta T cell (ENCSR019HQR)

summary:
H3K9me3 ChIP-seq on CD4-positive, alpha-beta T cell male adult (20 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from IgD-negative memory B cell (ENCSR119PSR)

summary:
H3K36me3 Mint-ChIP-seq on human IgD-negative memory B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from brain (ENCSR019BOC)

summary:
H3K4me3 Mint-ChIP-seq on human H9 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR119DDY)

summary:
H3K4me1 Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive B cell (ENCSR119CTT)

summary:
Control Mint-ChIP-seq on human naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive B cell (ENCSR115FGJ)

summary:
H3K4me3 Mint-ChIP-seq on human naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR116FVG)


title: Mint-ChIP-seq from excitatory neuron (ENCSR212HWF)

summary:
H3K9me3 Mint-ChIP-seq on human PGP1 derived excitatory neuron

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR131SAQ)

summary:
Control Mint-ChIP-seq of CD4-positive, alpha-beta memory T cell originated from CD4-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from HFFc6 (ENCSR114FEG)

summary:
Control Mint-ChIP-seq on human HFFc6

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR114AZZ)

summary:
H3K36me3 Mint-ChIP-seq on human CD4-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR018JXB)

summary:
H3K36me3 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive B cell (ENCSR111MNI)


title: Control Mint-ChIP-seq from immature natural killer cell (ENCSR204YIP)

summary:
Control Mint-ChIP-seq on human immature natural killer cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from neural progenitor cell (ENCSR211MKD)

summary:
H3K27ac Mint-ChIP-seq on human H9 derived neural progenitor cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR207GLV)

summary:
ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from neural progenitor cell (ENCSR010GRX)

summary:
Control Mint-ChIP-seq on human H9 derived neural progenitor cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from HCT116 (ENCSR012LAX)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR205FKJ)

summary:
Control Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR209ADM)


title: Mint-ChIP-seq from CD8-positive, alpha-beta memory T cell (ENCSR112KIE)

summary:
H3K27me3 Mint-ChIP-seq on human CD8-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD8-positive, alpha-beta T cell (ENCSR209TVI)

summary:
H3K36me3 Mint-ChIP-seq of CD8-positive, alpha-beta T cell male adult (21 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from nephron (ENCSR007ZSS)

summary:
H3K27ac Mint-ChIP-seq on human H9 derived nephron organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from endodermal cell (ENCSR110OND)

summary:
H3K36me3 Mint-ChIP-seq on human H9 derived endodermal cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from brain (ENCSR106WDX)

summary:
Control Mint-ChIP-seq on human PGP1 derived brain organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from SK-N-SH (ENCSR209FGM)

summary:
ChIP-seq on human SK-N-SH

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from type B pancreatic cell (ENCSR204EXQ)


title: Mint-ChIP-seq from CD8-positive naive resting alpha-beta T cell (ENCSR105REF)


title: Mint-ChIP-seq from T-cell (ENCSR006CYO)

summary:
H3K27me3 Mint-ChIP-seq of T-cell male adult (42 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from nephron (ENCSR007HIL)

summary:
H3K36me3 Mint-ChIP-seq on human H9 derived nephron organoid

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive B cell (ENCSR104CUK)

summary:
H3K36me3 Mint-ChIP-seq on human naive B cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR005BTU)

summary:
H3K27ac Mint-ChIP-seq on human naive thymus-derived CD8-positive, alpha-beta T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control Mint-ChIP-seq from T-cell (ENCSR203XDG)

summary:
Control Mint-ChIP-seq on T-cell male adult (38 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from K562 (ENCSR004LZA)


title: Control Mint-ChIP-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR201SEO)

summary:
Control Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (43 years) treated with 10 ng

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR002UMT)

summary:
H3K27me3 ChIP-seq on CD4-positive, alpha-beta memory T cell male adult (43 years)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR101USF)


title: Mint-ChIP-seq from endodermal cell (ENCSR102GPT)

summary:
H3K9me3 Mint-ChIP-seq on human H9 derived endodermal cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR003SWN)

summary:
H3K27ac Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (43 years) treated with anti-CD3 and anti-CD28 coated beads

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from excitatory neuron (ENCSR201NXK)

summary:
H3K4me1 Mint-ChIP-seq on human PGP1 derived excitatory neuron

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR200SSJ)

summary:
H3K27ac Mint-ChIP-seq of CD4-positive, alpha-beta memory T cell originated from CD4-positive, alpha-beta memory T cell

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Mint-ChIP-seq from naive B cell (ENCSR200JRA)


title: Mint-ChIP-seq from activated CD4 positive, naive alpha-beta T cell (ENCSR100CMZ)

summary:
H3K27ac Mint-ChIP-seq of activated CD4-positive, alpha-beta T cell male adult (43 years) treated with 10 ng

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Contiguous Erosion of the Inactive X in Human Pluripotency Concludes With Global DNA Hypomethylation

city: Farmington

first: Stefan

middle: F

last: Pinter

state: CT

address: 263 Farmington Avenue

department: Genetics and Genome Sciences

institute: University of Connecticut, UConn Health

type: Methylation profiling by genome tiling array

summary:
Female human pluripotent stem cells (hPSCs) are prone to undergoing X chromosome erosion (XCE), a progressive loss of key epigenetic features on the inactive X that initiates with repression of XIST, the long non-coding RNA required for X inactivation. As a result, previously silenced genes on the eroding X (Xe) reactivate, some of which are thought to provide selective advantages. To-date, the sporadic and progressive nature of XCE has largely obscured its scale, dynamics, and key transition events.
To address this knowledge gap, we performed an integrated analysis of DNA methylation (DNAme), chromatin accessibility, and gene expression across hundreds of hPSC samples. Differential methylation across the Xe enables ordering female hPSCs across a trajectory of XCE from initiation to terminal stages. Our results identify a crucial cis-regulatory element for XIST expression, trace contiguously growing domains of reactivation to a few euchromatic origins on the Xi, and indicate that the late-stage Xe impairs DNAme genome-wide. Surprisingly, from this altered epigenetic landscape emerge select features of naïve pluripotency, suggesting its link to X chromosome dosage may be partially conserved in human embryonic development.

overall_design: Bisulfite-converted DNA from the 22 samples were hybridised to the Illumina Infinium methylEPIC (850K) Human Methylation BeadChip.

first: Prakhar

last: Bansal

first: Darcy

middle: T

last: Ahern

first: Yuvabharath

last: Kondaveeti

first: Catherine

middle: W

last: Qiu


title: Analysis of Differentially Expressed Genes in sorted CD4+ CD8+ doubl positive (DP) thymocytes from wild type (WT) and NSRP1CD4Cre (KO) mice

city: Gwangju

first: Chang-Hyun

last: Kim

address: 123, Cheomdangwagi-ro, Buk-gu

department: School of Life Sciences

country: South Korea

institute: Gwangju Institute of Science and Technology (GIST)

summary: NSrp70 deficiency (NSRP1f/fCD4Cre) profoundly perturbed the late development of DP thymocytes, leading to a significant reduction of single positive (SP) cells in the thymus and peripheral lymphoid tissues. To gain further insight how NSrp70 controls thymocyte development from DP stage, we performed RNA-seq analysis after sorting DP thymocytes from WT and Nsrp1 cKO mice.

overall_design: Gene profiles differentially expressed in NSRP1-deficient DP thymocytes compare to wild-type thymocytes

first: Sang-Mu

last: Park

first: Hye-Ran

first: Young-Dae

first: Chang-Duk

last: Jun


title: ERK signaling mediates resistance to immunomodulatory drugs in the bone marrow microenvironment (CRISPR Screen)

city: Boston

first: Jiye

last: Liu

state: MA

address: 450 Brookline Ave

department: Medical Oncology

institute: Dana-Farber Cancer Institute

summary: Immunomodulatory drugs (IMiDs) have markedly improved patient outcome in multiple myeloma (MM); however, resistance to IMiDs commonly underlies relapse of disease. Here we identify and validate that TNF receptor associated factor protein family TRAF2 KD/KO in MM cells mediates IMiDs resistance via activation of non-canonical NF-kB and MEK-ERK signaling. Within MM bone marrow (BM) stromal cell supernatants, TNF-a induces proteasomal degradation of TRAF2, non-canonical NF-kB, and downstream ERK signaling in MM cells, whereas IL-6 directly triggers ERK activation. RNA sequencing of MM patient samples shows nearly universal ERK pathway activation at relapse on lenalidomide maintenance therapy, confirming its clinical relevance. Combination MEK inhibitor treatment restores IMiDs sensitivity of TRAF2 KO cells both in vitro and in vivo using an inducible TRAF2 KD MM xenograft model. Our studies provide the framework for clinical trials of MEK inhibitors to overcome IMiDs resistance in the BM microenvironment and improve patient outcome in MM.

overall_design: Genome-wide CRISPR/cas9 screening in MM1S cells for Pomalidomide resistance

first: Su

last: Wang

first: Kenneth

last: Anderson


title: A transcribed ultra-conserved noncoding RNA, uc.285+, promotes colorectal cancer proliferation via directly binding mRNA

city: Nanning

first: Aruo

state: Guangxi

address: Guangxi Medical University, Nanning 530021, Guangxi, China

country: China

institute: Guangxi Medical University

summary: To further explore the differential expression profile of Transcribed ultra-conserved region (TUCR) in human colorectal cancer, we have employed TUCR microarray expression profiling as a discovery platform to identify potential differential expression profile of TUCR between human colorectal cancer tissue (CCRT) and human normal mucosal epithelial tissue of the colorectal (NT). Results showed that multiple differentially expressed TUCRs were found between CCRT and NT. In this study, We selected T-UCRs with large differences to verification and found that uc.285+ upregulation was most obvious. Then we further explored the biological function and mechanism of uc.285+ in colorectal cancer.

overall_design: In the initial stage, we conducted a Transcribed ultra-conserved region (TUCR) microarray analysis using human colorectal cancer tissue (CCRT) and human normal mucosal epithelial tissue of the colorectal (NT). Then we find out the differentially expressed TUCRs, and explore its function and mechanism of action through molecular biology experiments in vivo and in vitro.

first: Ruirui

last: Zhang

first: Shuilian

last: Wu

first: Xin


title: RNA-seq of mouse Pmel-1 CD8 T cell with Ucp2 inhibition and NAC treatment

city: Bethesda

first: Eytan

last: Ruppin

address: 9000 Rockville Pike

institute: National Institutes of Health

summary: Enhanced T cell stemness and anti-tumor activity of adoptively transferred T cells are linked to T cell metabolism, however, the mitochondrial regulation of T-cell longevity and anti-tumor activity remains elusive. Here, using loss and gain of function experiments, we show that a mitochondrial inner membrane protein, Uncoupling protein 2 (Ucp2), is required for T cell longevity and anti-tumor function. Loss of mitochondrial Ucp2 activity in T cells results in accelerated differentiation into ‘terminal effector cells’. We found that Ucp2 modulate oxidative stress and DNA damage by regulating the levels of mitochondrial superoxide. We observed that reducing mitochondrial ROS was sufficient to rescue the loss of Ucp2-mediated increase in effector T cell differentiation, senescence, cytokine production and anti-tumor activity. Tumor-specific CD8+ T cells could be metabolically reprogrammed by increasing Ucp2 levels and Ucp2-overexpressing T cells displayed long-term survival and restricted tumor growth and prolonged the survival of melanoma-bearing mice. Our results establish a novel role of Ucp2 in regulating T cell longevity and anti-tumor activity by repressing mitochondrial dysfunction and suggest that manipulating Ucp2 levels in T cells should enhance T cell-based immunotherapies for cancer.

overall_design: CD8+ T cells from pmel-1 mice were stimulated in vitro with 1 μM hgp10025–33 peptide or plate-bound anti-CD3 (2 μg/ml; 145-2C11; BD Biosciences) and soluble anti-CD28 (1 μg/ml; 37.5 l; BD Biosciences) and expanded in culture medium containing 10 ng•ml–1 IL-2 (Chiron) for 4 days. T cells were incubated with genipin, or NAC (Sigma-Aldrich) or vehicle (culture media) at various indicated doses, with three replicates in each experimental group. RNA was extracted from the T cells with Illumina TruSeq Stranded Total RNA library preparation kit and subject to sequencing on Illumina HiSeq3000/4000.

first: Sukumar

last: Madhusudhanan

first: Cheng

last: Kuoyuan

first: Vodnala

last: Suman

first: Restifo

last: Nicholas

first: Ruppin

last: Eytan


title: The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct from its DNA-binding function in Ewing sarcoma [RNA-seq III]

city: Columbus

first: Megann

middle: A.

last: Boone

state: OH

address: 700 Children's Drive, WA5011

department: Center for Childhood Cancer

institute: Nationwide Children's Hospital

summary: The purpose of this study was to determine transcriptional regulatory activity of EWS/FLI mutants in an alternative, non-Ewing sarcoma cell line. EWS/FLI cDNA constructs including various deletions of the FLI portion were transfected in HEK-293EBNA cells and we sought to determine the transcriptional profile of each through RNA-sequencing.

overall_design: EWS/FLI cDNA constructs were transfected and expressed in HEK-293EBNA cells. Cells were collected after 48 hours post-transfection and total RNA was extracted to study the transcriptomic profiles of each EWS/FLI construct. 3 biological replicates were performed for this experiment.

middle: A

first: Cenny

last: Taslim

first: Stephen

middle: L

last: Lessnick


title: Gene expression analysis of control and Dnmt1 null Pdgfrb-positive myofibroblasts in 7 days old mice.

city: Los Angeles

first: Brendan

middle: H

last: Grubbs

address: 4661 W. Sunset Blvd.

department: Obstetrics and Gynecology

institute: University of Southern California

summary: Background  DNA methylation is an epigenetic mark that restricts chromatin accessibility and serves to modulate temporal and spatial gene expression during organogenesis. Dnmt1 is one of the most studied DNA methyltransferases, and it is primarily involved in preserving the DNA methylation pattern in cells undergoing mitotic division. While the role of Dnmt1 in the embryonic lung endoderm has been revealed, its role in expansion, maintence and differentiation of the embryonic lung mesoderm is mostly unknown. Here, we present the first evidence showing that Dnmt1 is necessary for the proper development of the embryonic lung mesoderm. By selectively deleting Dnmt1 in the embryonic lung mesoderm we found that Dnmt1 is critical for the development of embryonic vasculature and fully commitment of mesoderm towards the lung mesenchymal cell lineages.  Results  Dnmt1 deletion in the embryonic lung mesenchyme at the E7.5 stage led to a lethal phenotype which was characterized by bilateral lung hypoplasia, impaired lung branching morphogenesis, and widespread hemorrhages in the parenchyma. The genesis of the hemorrhages was likely a result of halted development of lung vasculature, specifically the ontogeny of pericytes, which was detected in the mutant lungs. However, despite the severe mesenchyme alteration, differentiation of the lung endoderm appeared normal. When Dnmt1 was deleted at later developmental periods (E13.5), the lung matured normally and mutant pups were viable, although reduced differentiation of Pdgfr- myofibroblasts and alveolar simplification were observed in all mutant animals as soon as 7 days after birth. Gene expression profiling studies revealed that deletion of Dnmt1 induced the ectopic expression of genes specific for testis, placenta, and ovary, such as Tex10.1, Tex19.1 and Pet2 which suggested a loss of commitment of the lung mesoderm toward the pulmonary cell lineages.   Conclusions  Taken together our findings have shown that dnmt1 expression in the mesenchyme of the developing lung is crucial for restricting the differentiation capacity of the pulmonary mesoderm and, thus, ensuring the adequate differentiation of vasculature cells and myofibroblasts in the fetal and postnatal lung.

overall_design: Examination of gene expression changes in wild type and Dnmt1-null neonal (P7) lung myofibroblasts.

first: Gianluca

last: Turcatel

first: Matthew

middle: E

last: Thornton

first: Priscilla

last: Munguia


title: Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4+ endothelial cells

city: Zurich

first: Hubert

last: Rehrauer

address: Winterthurerstr. 190

department: FGCZ

country: Switzerland

institute: ETH Zurich / University of Zurich

summary: Exercise is a powerful driver of physiological angiogenesis during adulthood, but the mechanisms of exercise-induced vascular expansion are poorly understood. We explored endothelial heterogeneity in skeletal muscle and identified two capillary muscle endothelial cells (mEC) populations which are characterized by differential expression of ATF3/4. Spatial mapping showed that ATF3/4 + mECs are enriched in red oxidative muscle areas while ATF3/4 low ECs lie adjacent to white glycolytic fibers. In vitro and in vivo experiments revealed that red ATF3/4 + mECs are more angiogenic when compared to white ATF3/4 low mECs. Mechanistically, ATF3/4 in mECs control genes involved in amino acid uptake and metabolism and metabolically prime red (ATF3/4 + ) mECs for angiogenesis. As a consequence, supplementation of non-essential amino acids and overexpression of ATF4 increased proliferation of white mECs. Finally, deleting Atf4 in ECs impaired exercise-induced angiogenesis. Our findings illustrate that spatial metabolic angiodiversity determines the angiogenic potential of muscle ECs.

overall_design: mRNA from sorted skeletal muscle (glycolytic or oxidative) endothelial cells (mECs) (CD31+CD45-) of WT and ATF4-/- mice (EC specific KO). 5 replicates per sample.

first: Zheng

last: Fan

first: Guillermo

last: Turiel

first: Raphaela

last: Ardicoglu

first: Moheb

last: Ghobrial

first: Evi

last: Masschelein

first: Tea

last: Kocijan

first: Jing

first: Ge

last: Tan

first: Gillian

last: Fitzgerald

first: Tatiane

last: Gorski

first: Abdiel

last: Alvarado-Diaz

first: Paola

last: Gilardoni

first: Christopher

middle: M

last: Adams

first: Bart

last: Ghesquière

first: Katrien

last: DeBock


title: Gene expression analysis of control and Dnmt1 CKO E18.5 murine lungs.

first: Brendan

last: Grubbs

overall_design: Examination of gene expression changes  in wild type and Dnmt1 CKO E18.5 lungs. 3 wildtype, 6 mutant (3 with weak phenotype, 3 with strong phenotype) lungs were utilized. Mutant lungs with weak phenotype were only hypoplastic.  Mutant lungs with strong phenotype were hypoplastic and displayed widespread hemorrhages within the parenchyma.

first: Gianluca

last: Turcatel

first: Matthew

last: Thornton

first: Priscilla


title: Single cell next generation sequencing of wild type and Dnmt1 conditional knock in  E18.5 embryonic lung

overall_design: Examination of gene expression changes at the single cell level in wild type and dnmt1-null embryonic murine lungs.

last: Munguia


title: EGFR-HIF1α signaling positively regulates the differentiation of IL-9 producing T helper cells

city: Faridabad

first: Abhay

middle: Deep

last: Pandey

address: 3rd Milestone, Faridabad-Gurgaon Expressway

department: Virology

country: India

institute: Regional Centre for Biotechnology

summary: Interleukin 9 (IL-9)-producing helper T (Th9) cells are essential for inducing anti-tumor immunity and inflammation in allergic and autoimmune diseases. Although transcription factors that are essential for Th9 cell differentiation have been identified, other signaling pathways that are required for their generation and functions are yet to be found. Here we identified that Epidermal Growth Factor Receptor (EGFR) is essential for IL-9 induction in Th cells. Moreover, amphiregulin (Areg), an EGFR ligand, is critical for the amplification of Th9 cells induced by TGF-β1 and IL-4. Furthermore, our data show that AREG-EGFR signaling induces HIF1α, which binds and transactivates IL-9, IRF4 and NOS2 promoters in Th9 cells. Loss of EGFR or HIF1α abrogates Th9 cell differentiation and suppress their anti-tumor functions. Moreover, in line with its reliance on HIF1α expression, metabolomics profiling of Th9 cells revealed that succinate, a TCA cycle metabolite, promotes Th9 cell differentiation and Th9 cell-mediated tumor regression.

overall_design: RNASeq analysis of Th9 cells from WT and Areg-/- mice.

first: Suyasha

last: Roy

first: Zaigham

last: Rizvi

first: Alexander

middle: J

last: Clarke

first: Felicity

last: Macdonald

first: Abhaydeep

first: Dietmar

last: Zaiss

first: Anna

middle: K

last: Simon

first: Amit

last: Awasthi


title: ERK signaling mediates resistance to immunomodulatory drugs in the bone marrow microenvironment

first: Jiye

last: Liu

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct from its DNA-binding function in Ewing sarcoma [RNA-seq II]

first: Megann

last: Boone

summary: The purpose of this study was to determine the roles of the alpha-helical region just downstream of the FLI ETS DNA-binding domain in EWS/FLI-driven gene regulation of Ewing sarcoma cells. EWS/FLI cDNA constructs including various deletions of the FLI portion were virally transduced into cells and we sought to determine the transcriptional profile of each.

overall_design: Endogenous EWS/FLI was knocked-down in the Ewing sarcoma A673 cell line and EWS/FLI cDNA constructs were expressed in these cells. Cells were collected after 8 days and total RNA was extracted to study the transcriptomic profiles of each EWS/FLI construct. 3 biological replicates were performed for this experiment.

first: Cenny

last: Taslim

first: Stephen

last: Lessnick


title: ERK signaling mediates resistance to immunomodulatory drugs in the bone marrow microenvironment (RNA-Seq)

overall_design: RNA-seq in MM1S wildtype and TRAF2 KO cells

first: Su

last: Wang

first: Kenneth

last: Anderson


title: The expression profiles of exosomal miRNAs associated with resistance to osimertinib (AZD9291) in EGFR-mutant NSCLC cells

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: 10-1 tebiro 6-chome

country: Japan

institute: Toray Industries,Inc.

summary: Exosomal miRNAs involved in resistance to osimertinib in EGFR-mutant NSCLC cells were successfully identified through the microoarray analysis.

overall_design: In this study, exosomes isolated from 4 EGFR-mutant lung adenocarcinoma cell lines were used to acquire expression profiles of exosomal miRNAs associated with resistance to osimertinib.

first: Kakeru

last: Hisakane

first: Masahiro

last: Seike


title: Single cell RNAseq of human nail unit defines RSPO4 onychofibroblasts and SPINK6 nail epithelium

city: Seoul

first: Jong Hee

last: Lee

address: 81, Irwon-ro, Gangnam-gu

department: Department of Dermatology

institute: Samsung Medical Center

summary: Here, we studied transcriptome profiles of human nail units from polydactly samples. Single cell RNAseq with 11,541 cells from 4 extra digits revealed nail-specific mesenchymal and epithelial cell populations

overall_design: We profiled transcriptomes of nail unit from 4 fresh human polydactyly specimens using single cell RNAseq (scRNAseq). Extra-digits from 6-12 months old patients were delivered to the dermatologic clinic immediately after the digit removal. All samples containing nail mesenchyme and epithelium were minced and dissociated within 3 hours of digit removal.

first: Dongyoun

first: Hyun-Je

last: Kim

first: Joon-Ho

last: Shim


title: CBX7 is a tumour suppressor that inhibits bladder cancer

city: shanghai

first: HUANG

middle: ZHENG

state: shanghai

address: hongkou district

institute: shanghai jiaotong university

summary: The Polycomb Group Proteins (PcG) are epigenetic regulatory complexes, dysregulation of which has been associated with multiple biological processes, including maintenance of cell identity, differentiation, proliferation, and cancer progression.PcGs form two multiprotein complexes, Polycomb repressive complex 1 (PRC1) and PRC2(1).The PRC2 protein complex mainly consists of Early embryonic deficient (EED), Suppressor of Zeste (SUZ12) and Enhancer of Zeste (EZH), which can catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3), thereby leaving a transcriptionally repressive mark on the chromatin . Such alterations are recognized and read by canonical PRC1 which is composed of CBX (polycomb), PCGF (polycomb group factor), HPH (human polyhomeotic homolog), and the E3-ligase protein (RING) that catalyzes the monoubiquitination of histone H2A on lysine 119 (H2AK119ub1). The H3K27me3 mark is identified by and binds to the chromodomain within the CBX protein in PRC1, thereby ubiquitinating H2AK119 via the RING proteins. The interaction of PRC2 and PRC1 in chromatin contributes to chromatin compaction and transcriptional silencing of target genes.There are five chromobox proteins in humans, CBX2, 4, 6, 7 and 8. Increasing evidence supports essential roles of CBX proteins in tumorigenesis. Remarkably, CBX proteins have shown an opposite function in distinct cancer types in tumor development. For example, CBX7 is overexpressed in ovarian and prostate cancer , implying its oncogenic role in these tumor types. In contrast, CBX7 functions as a tumor suppressor and loss of CBX7 has been associated with increasing the malignancy grade in bladder, breast, pancreatic, glioma, and colon carcinomas (3 4 5 6 7), but its tumor suppression mechanism is unclear.

overall_design: Transcriptome analysis of T24 cell line expressing CBX7 protein.

first: Zhengnan

last: Huang

first: Jun

last: Yan


title: Cytomegalovirus subverts macrophage identity [LysMcreZeb1flox_vs_LysMcreZeb1wt]

city: Freiburg

first: Sebastian

last: Baasch

address: Breisacher Str.

department: Institute for Immunodeficiency; Center for Chronic Immunodeficiency

country: Germany

institute: University Medical Center

summary: Macrophages, which populate barrier tissues already in the embryo, are primary targets for CMV. Upon infection macrophages undergo a morphological, immunophenotypic and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness and provision of the cell cycle machinery to viral proliferation.

overall_design: mRNA Transcriptomes of infected alveolar macrophages at 3dpi were prepared in biological triplicates.


title: Genome-wide analysis of human endometria

city: Nanjing

first: Minmin

last: Song

address: 321 Zhongshan Rd.

institute: The Affiliated Drum Tower Hospital of Nanjing University Medical School

type: Non-coding RNA profiling by high throughput sequencing

summary: Intrauterine adhesions (IUA) are the most common reason of uterine infertility, which is characterized by partial or complete closure of uterine cavity and endometrial progressive fibrosis. This disease is often secondary to uterine curettage or other intrauterine surgery. The clinical manifestations include hypomenorrhea even amenorrhea, infertility or recurrent spontaneous abortion. In this work, endometria samples were collected from IUA and control patients. RNA-seq was performed to identify differences in circRNAs and miRNAs expression. This study may provide further insight in the mechanisms of IUA and function as preventive, predictive and therapeutic measures.

overall_design: Endometria samples from 3 IUA patients (Ba) and 3 normal controls (Con)

first: Yali

last: Hu


title: mTORC1 Activation is not sufficient to suppress hepatic PPAR-a signalling or ketogenesis

city: Baltimore

first: Michael

last: Wolfgang

state: Maryland

address: 820 N Wolfe St, Rangos Building, 480.14

department: Biological Chemistry

institute: Johns Hopkins School of Medicine

summary: we examined if the activation of the anabolic program mediated by the activation of the mTorc1 complex in the fasted state could suppress the robust catabolic programing and enhanced Pparα transcriptional of mice with a liver specific defect in mitochondrial long chain fatty acid oxidation (Cpt2L-/- mice). We found that the activation of mTorc1 in the fasted state was not sufficient to repress Pparα responsive genes or ketogenesis.

overall_design: Examination of PPAR-a signalling and ketogenesis through knock-out mouse models. Data collected from chow fed, 24-hour fasted male mouse livers.

first: Ebru

last: Selin Selen

first: Kyle

last: Cavagnini


title: Single-cell transcriptomic analysis of day 100 multilineage and gut organoids

city: San Francisco

first: Todd

last: McDevitt

address: 1650 Owens St

department: GICD

institute: Gladstone Institutes

summary: Single-cell RNA-sequencing was used to characterize the cellular diversity of dissociated cells from day 100 multilineage and gut organoids.

overall_design: Organoids at day 100.

first: Ana

middle: C

last: Silva

first: David

last: Joy


title: Retrospective analysis of mesendoderm progenitors that give rise to cardiac microtissues, multilineage and gut organoids

summary: Bulk RNA-sequencing of the mesendoderm progenitors before aggregation. Mesendoderm progenitors aggregates can lead to the formation of cardiac microtissues, multilineage and gut organoids in different batches. Despite batch-to-batch differences in spheroid phenotype, all spheroids (n>200) within a single batch derived from the same initial differentiation of progenitor cells manifested identical morphologies and cellularity.

overall_design: Mesendoderm progenitors at differentiation day 5.

first: Mara

last: Kauss

first: Vaishaali

last: Natajaran

last: Alexanian

first: Benoit

middle: G

last: Bruneau


title: Transcriptome analysis of the scleroderma skin tissue treated with BMSC derived exosome in mouse

city: Shanghai

first: Qingjian

last: Ou

address: Siping Rd

department: Medical

institute: Tongji University

summary: We aim to explore the transcriptome of the dermis of the bleomycin induced murine scleroderma model which were treated with PBS or bone marrow stem cell derived exosome.

overall_design: The bleomycin induced murine scleroderma model were treated with BMSC derived exosome or PBS for 7days.


title: p38α activation-mediated IFNAR1 downregulation by tumor derived factors induced neutrophil-attracting chemokines production

city: PHILADELPHIA PA

last: Gui

state: PA

address: 380 S UNIVERSITY AVE HILL 345

department: School of Veterinary Medicine

institute: UNIVERSITY OF PENNSYLVANIA

summary: Tumor derived factors induced type I interferon receptor (IFNAR1) downregulation both in vivo and in vitro. IFNAR1 was shown to be phosphorylated, ubiquitinated and downregulated in response to soluble or vesicular tumor derived factors in a p38-dependent manner. Upon administration of B16F10 tumor derived factors, lungs of Ifnar1S526A knock-in mice (termed "SA"), where mutation in a phospho-acceptor site within the IFNAR1 phospho-degron renders IFNAR1 insensitive to p38-driven phosphorylation, ubiquitination and degradation, retained IFNAR1 and sustained the expression of the IFN stimulated genes. Futuremore, careful examination and validation of gene expression profiles revealed an increased expression of several chemokines known to attract neutrophils (including Cxcl1, Cxcl3 and Cxcl5) in the lungs of  WT mice treated with tumor derived factors. This increase was notably less pronounced in the SA mice, suggesting that IFNAR1 downregulation by tumor derived factors induced neutrophil-attracting chemokines production.

overall_design: Two biological replicates were analyzed for each of two genotypes (WT and SA)

first: Daniel

last: Beiting


title: Transcriptome analysis the miRNA of exosome derived from mouse bone marrow stem cell

summary: We aim to explore the types and expression of miRNA in the mouse bone marrow stem cell derived exosome.

overall_design: Two mouse bone marrow stem cell derived exosome samples were analyzed with miRNA sequencing.

first: Jiahui

last: Jin


title: The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct from its DNA-binding function in Ewing sarcoma [CUT&RUN]

first: Megann

last: Boone

summary: The purpose of this study was to compare the relevance of the FLI portion for genomic localization of the EWS/FLI protein in Ewing sarcoma cells. EWS/FLI cDNA constructs including various deletions of the FLI portion were virally transduced into cells and we sought to determine the ATAC profile of each.

overall_design: Endogenous EWS/FLI was knocked-down in the Ewing sarcoma A673 cell line and EWS/FLI cDNA constructs were expressed in these cells. Cells were collected after 8 days and antibody-directed micrococcal nuclease was used to determine the binding locations of these EWS/FLI protein constructs. Two biological replicates for each sample were used to construct cDNA libraries; each library was submitted twice to acheive sufficient read-depth and combined for analysis.

first: Cenny

last: Taslim

first: Stephen

last: Lessnick


title: The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct from its DNA-binding function in Ewing sarcoma [ATAC-seq]

summary: The purpose of this study was to compare the relevance of the FLI portion of EWS/FLI in the ability of the protein to act as a pioneer factor in Ewing sarcoma cells. EWS/FLI cDNA constructs including various deletions of the FLI portion were virally transduced into cells and we sought to determine the ATAC profile of each.

overall_design: Endogenous EWS/FLI was knocked-down in the Ewing sarcoma A673 cell line and EWS/FLI cDNA constructs were expressed in these cells. Cells were collected after 8 days and ATAC was performed using Tn5 to detemrine the ability of each to EWS/FLI construct to alter chromatin state.

first: Meng

last: Wang


title: Opposing tumor promoting and suppressive functions of Rictor/mTORC2 signaling in adult glioma and pediatric SHH medulloblastoma

city: Heidelberg

first: Marcel

last: Kool

address: Im Neuenheimer Feld 280

department: Pediatric Neurooncology

institute: German Cancer Research Center DKFZ

summary: Most human cancers arise from stem/progenitor cells by sequential accumulation of genetic/epigenetic alterations, while cancer modeling typically requires simultaneous multiple oncogenic events. Here we show that a single p53 mutation, despite causing no defect in mouse brain, promoted neural stem/progenitor cells to spontaneously accumulate oncogenic alterations, including loss of multiple chromosomal (chr) regions syntenic to human chr10 containing Pten, forming malignant gliomas/glioblastomas with PI3K/Akt activation. Rictor/mTORC2 loss inhibited Akt signaling, greatly delaying and reducing glioma formation by suppressing glioma precursors within the subventricular zone stem-cell niche. Unexpectedly, Rictor/mTORC2 loss delayed timely differentiation of granule cell precursors (GCPs) during cerebellar development, promoting sustained GCP proliferation and medulloblastoma formation, which recapitulated critical features of TP53-mutant Sonic Hedgehog (SHH) medulloblastomas with GLI2 and/or N-MYC amplification. Our study demonstrates that Rictor/mTORC2 has opposing functions in neural stem cells and GCPs in the adult and developing brain, promoting malignant gliomas/glioblastoma and suppressing SHH-medulloblastoma formation, respectively.

overall_design: 22 mouse medulloblastomas, 6 mouse gliomas and 24 normal mouse brain tissues were profiled on the Affymetrix Mouse Genome mm430.2 array.

first: Yuan

last: Zhu

first: Seçkin

last: Akgül


title: Cytomegalovirus subverts macrophage identity [Alveolar macrophages]

first: Sebastian

last: Baasch

overall_design: mRNA Transcriptomes of control, bystanding (non-infected) and infected alveolar macrophages at 3dpi were prepared in biological triplicates.


title: A Multi-Omics Analysis of Mucosal-Associated-Invariant T cells reveals key drivers of distinct modes of activation

city: Leipzig

first: Jana

last: Schor

state: Saxony

address: Permoserstr. 15

department: Molecular Systems Biology

institute: Helmholtz Centre for Environmental Research

summary: The function of mucosal-associated invariant T (MAIT) highly depends on the mode of activation, either by recognition of bacterial metabolites via their T cell receptor (TCR) or in a TCR-independent manner via cytokines. The underlying molecular mechanisms are not entirely understood. To define the activation of MAIT cells on the molecular level, we applied a multi-omics approach with untargeted transcriptomics, proteomics and metabolomics.  Transcriptomic analysis of E.coli- and TCR-activated MAIT cells showed a distinct transcriptional reprogramming, including altered pathways, transcription factors and effector molecules. We validated the consequences of this reprogramming on the phenotype by proteomics and metabolomics. Thus, and to distinguish between TCR-dependent and -independent activation, MAIT cells were stimulated with IL12/IL18, anti-CD3/CD28 or both. Only a combination of both led to full activation of MAIT cells, comparable to activation by E.coli. Using an integrated network-based approach, we identified key drivers of the distinct modes of activation, including cytokines and transcription factors, as well as negative feedback regulators like TWIST1 or LAG3. Taken together, we present novel insights into the biological function of MAIT cells, which may represent a basis for therapeutic approaches to target MAIT cells in pathological conditions.

overall_design: Control samples: 5 MAITcells at 0h timepoint, 5 unstimulated MAITcells at 16h timepoint, 5 at 16h timepoint after activation via E.coli and 5 at 16h timepoint TCR-activated MAITcells

first: Kristin

last: Schubert

first: Isabel

last: Karkossa

first: Beatrice

last: Engelmann

first: Lisa

last: Steinheuer

first: Ulrike

last: Rolle-Kampczyk

first: Jörg

last: Hackermüller

first: Martin

last: von Bergen


title: A role for the ribosome-associated complex in activation of the IRE1 branch of UPR

status: Public on Jun 14 2021

city: Lexington

first: Jae Seok

last: YOON

address: 44 Hartwell Avenue

department: CFFT Lab

institute: Cystic Fibrosis Foundation

summary: The ubiquitous ribosome-associated complex (RAC) is a chaperone that spans ribosomes, making contacts near both the polypeptide exit tunnel and the decoding center, a position prime for sensing and coordinating translation and folding. Loss of RAC is known to result in growth defects and sensitization to translational and osmotic stresses. However, the physiological substrates of RAC and the mechanism(s) by which RAC is involved in responding to specific stresses in higher eukaryotes remain obscure. Data presented here uncover an essential function of mammalian RAC in the unfolded protein response (UPR). Knockdown of RAC sensitizes mammalian cells to ER stress and selectively interferes with IRE1 branch activation. Higher-order oligomerization of the IRE1α kinase/endoribonuclease depends upon RAC. These results reveal a surveillance function for RAC in the UPR: modulating IRE1α clustering as required for endonuclease activation and splicing of the substrate Xbp1 mRNA.

overall_design: Ribosome profiling of XBP1 in the Thapsigargin-induced ER stress condition in HEK293 cells

last: Yoon

first: I-Hui

last: Wu

first: William

last: Skach

first: Philip

last: Thomas


title: Sex-specific transcriptomic profiles and imprinting drive nicotine self-administration in rats and inform the genetic basis of human smoking behavior

city: Stanford

first: Robert

middle: Raymond

last: Butler

address: 3172 Porter Dr., MC 5475

department: Neurology & Neurological Sciences

institute: Stanford University School of Medicine

summary: Tobacco cigarette smoking, with nicotine (NIC) as the addictive component, is a large risk factor for human mortality. In animals, repeated NIC exposure leads to sensitization (SST) and enhances self-administration (SA) of NIC. However, the molecular basis of SST and SA and their genetic relevance to smoking behavior are poorly understood. Using F1 progeny of inbred Envigo rats (F344/BN), we carried out a transcriptional profiling of NIC SST and SA in ventral tegmental area (VTA), nucleus accumbens core (Nac) and shell (Nash). We observed male-specific NIC SST and a parental effect of NIC with SA only present in paternal F344 crosses. Gene differential expression (DE) analysis revealed sex and brain region-specific transcriptomic signatures of SST and SA, with genes downregulated in male VTA associated with both SST and SA, while genes upregulated in male Nac were associated with SA. DE genes associated with SST and SA are enriched for those related to synaptic processes, myelin sheath, and tobacco use disorder or chemdependency. Interestingly, we found that for SST the downregulated genes in the male VTA tended to be upregulated in female VTA, and the overlapping genes were strongly enriched for smoking genome-wide association study (GWAS) risk variants, which may thus explain male-specific SST. To gain mechanistic insight on the observed parental effect of SA, we analyzed the allelic imbalance of expression (AIE) in reciprocally crossed F1 rats that exhibited differential tendency of SA and found widespread region-specific AIE. For the SA-inclined rats, the genes showing AIE bias towards paternal F344 alleles in Nac were strongly enriched for genes upregulated in Nac DE—the gene set most relevant to NIC SA—and also for GWAS risk variants of smoking initiation. These findings show a prominent role for sex and region-specific gene expression and imprinting in NIC SST and SA, and suggest a mechanistic link between genes underlying these processes and human NIC addiction. This study provides a resource for understanding the biology underlying the genetic findings on human smoking phenotypes.

overall_design: F1 progeny were generated by crossing two inbred Envigo strains (Fischer-344 [F344] and Brown Norway [BN]). Initial cross (F1i) was performed by crossing male F344 and female BN. Reciprocal cross (F1r) was performed by crossing female F344 and male BN. The proven breeding pairs (F344/NHsd and BN/RijHsd) were purchased from Envigo. The breeding was carried out at the University of Chicago animal facility.     For self-administration, F1 males were administered NIC (0.4 mg/kg, IP; n=6) and SAL (1.0 ml/kg, n=6) every day for a total of 4 days.  Starting from day 7, NIC (n=4) and SAL (n=4) exposed rats received additional NIC injection intravenously every day (30µg/kg/infusion of NIC base = ~1.8 mg/kg) for 6 days. Therefore, the NIC self-administering rats were exposed to 6 (days) X 10 (infusions) = 60 infusions. This is roughly equivalent to what the passively administered rats received: 4 (days) X 0.4 mg/kg = 1.6 mg/kg. At each day SA test was performed by counting active lever presses for both NIC injected group and SAL control (2 NIC and 2 SAL exposed rats which did not receive additional IV NIC injections). For SA transcriptomic analysis brain tissues (~20mg) from Nac, Nash and VTA regions were harvested on day 15. transcriptomic analysis F1 males (n=16) and females (n=16) were divided in 2 groups. In the first group (n=8) rats were exposed to 0.4 mg/kg of NIC (base) every day for 4 days. In the second group (n=8) rats were exposed to SAL (1.0 ml/kg) every day for 4 days. Brain tissues (~20mg) from Nac, Nash and VTA regions were harvested on day 17.

middle: R

last: Butler III

first: Alena

last: Kozlova

first: Siwei

last: Zhang

first: Thomas

last: Ujas

first: Hanwen

first: Stephan

last: Steidl

first: Alan

last: Sanders

first: Zhiping

middle: P

last: Pang

first: Pablo

middle: V

last: Gejman

first: Paul

last: Vezina

first: Jubao

last: Duan


title: Dietary soyasaponin and prebiotics modulate intestinal health and function in the cleaner fish Ballan wrasse (Labrus bergylta)

city: Bergen

first: Kai

middle: Kristoffer

last: Lie

state: Hordaland

address: Pobox 2029 Nordnes

department: Feed Safety

country: Norway

institute: Institute of Marine research

summary: This paper presents data from a 5-week feeding trial in which Ballan wrasse was fed either a reference diet, or the identical diet supplemented with i) the antinutrient soya saponin (0.7%) ii) a commercial prebiotic (Aquate™ SG, 0.4%) or iii) a combination of soya saponin and prebiotics. Blood, tissue and gut content from four separate intestinal segments were sampled from 6 fish per duplicate tank. Gut health and digestive functions were evaluated by various endpoint measurements employing biochemical and histomorphological tools as well as global gene expression profiling. No significant differences in fish growth were seen between the four dietary groups. Saponin supplementation, both alone and in combination with prebiotics, increased weight indices of two mid gut segments (IN2 and IN3) and decreased blood plasma glucose, cholesterol and total protein. Dry matter of intestinal content and activity of digestive enzymes were not affected by diet. Histomorphological analyses revealed clear structural alterations in the gut of fish fed saponin, both alone and in combination with prebiotics. The results indicated a progressing inflammation with increased infiltration by immune cells particularly into the distal parts of the intestine. Gene expression profiles obtained by RNA sequencing and quantitative PCR mirrored the histological and biochemical changes induced by the saponin load. The work has provided novel basic knowledge on the anatomy, digestive and immune function of the Ballan wrasse intestine. Additionally, the study demonstrated that Ballan wrasse gut health and digestive function may be markedly affected by diet composition.

overall_design: Five week feeding trial with ballan wrasse fed fed either a control diet, controll+sapanonis, controll+prebiotics og controll+saponins+ prebiotics.

first: Weiwen

last: Zhou

first: Elvis

last: Chikwati

first: Katerina

last: Kousoulaki

first: Ingrid

last: Lein

first: Gerd

last: Sæle

first: Åshild

last: Krogdahl

first: Trond

last: Kortner


title: HIF1-driven transcriptional changes in the heart

city: Honolulu

first: Allison

middle: Lesher

last: Williams

state: HI - Hawaii

address: 651 Ilalo St BSB 311

institute: University of Hawaii

summary: Ischemic heart disease is a leading cause of heart failure and hypoxia inducible factor 1 (HIF1) has been shown to be a key transcription factor in the early response to hypoxic injury. We previously developed an inducble model of cardiomyopathy using cardiomyocyte-specific expression of a mutated, oxygen-stable form of HIF-1⍺ (HIF-PPN). In this study, we used high throughput sequencing to explore HIF1-mediated transcriptional changes in the heart.

overall_design: Male mice expressing a stable form of HIF-1α under control of the Tet-Off system were given water either containing doxycycline (ON) or after withdrawal from doxycycline for three days (3D). Control mice remained on doxycycline and while those off doxycycline expressed HIF-PPN. Hearts were isolated and flash frozen before RNA isolation. Three mice were used for each condition as biological replicates.

first: Chad

middle: B

last: Walton

first: Vedbar

middle: S

last: Khadka

first: K

middle: W

last: McMahon

first: Ralph

last: Shohet


title: Sex-specific transcriptomic profiles of nicotine sensitization in rats inform the genetic basis of human smoking behavior

first: Robert

last: Butler

overall_design: F1 progeny were generated by crossing two inbred Envigo strains (Fischer-344 [F344] and Brown Norway [BN]). Initial cross (F1i) was performed by crossing male F344 and female BN. Reciprocal cross (F1r) was performed by crossing female F344 and male BN. The proven breeding pairs (F344/NHsd and BN/RijHsd) were purchased from Envigo. The breeding was carried out at the University of Chicago animal facility.     For sensitization, F1 males (n=5-6/group) and females (n=7/group) were randomly assigned the to three groups and tested in early adulthood (~250 g). The first group received 0.1 mg/kg of NIC (base), the second group received 0.4 mg/kg of NIC (base) and the third group received SAL (1.0 ml/kg). F1 rats were daily administered either NIC or SAL for 4 days. On days 1 and 4, rats were placed in an open field immediately after the injection and their locomotion measured for 2 hours. Rats were then left undisturbed in their home cages for 2 weeks. On day 19, all F1 rats were administered one injection of NIC (0.4 mg/kg, IP, base), immediately placed in the open fields and their locomotion measured for two hours. For the SST transcriptomic analysis F1 males (n=16) and females (n=16) were divided in 2 groups. In the first group (n=8) rats were exposed to 0.4 mg/kg of NIC (base) every day for 4 days. In the second group (n=8) rats were exposed to SAL (1.0 ml/kg) every day for 4 days. Brain tissues (~20mg) from Nac, Nash and VTA regions were harvested on day 17.

last: Butler III

first: Alena

last: Kozlova

first: Siwei

last: Zhang

first: Thomas

last: Ujas

first: Hanwen

first: Stephan

last: Steidl

first: Alan

last: Sanders

first: Zhiping

last: Pang


title: Cytomegalovirus subverts macrophage identity [Bone marrow-derived macrophages]

first: Sebastian

last: Baasch

overall_design: mRNA Transcriptomes of control, bystanding (non-infected) and infected bone marrow-derived macrophages at 3dpi were prepared in biological triplicates.


title: Genome-wide analyses reveal the coordination between alternative splicing and DNA methylation for light response in plants

city: Taipei

first: Pao-Yang

last: Chen

address: 128 Sec. 2, Academia Rd, Nankang,

department: Institute of Plant and Microbial Biology

country: Taiwan

institute: Academia Sinica

type: Methylation profiling by high throughput sequencing

summary: In this study, we investigated the possibility that light regulates alternative splicing (AS) through modulating DNA methylation of specific gene loci. The bisulfite sequencing data were extensively evaluated with AS pattern from mRNA sequencing of samples with the same light treatment.

overall_design: One-week-old Arabidopsis seedlings were transferred to the dark for 3 days, and then irradiated under red or blue light for 1 and 4 hours. Genomic DNA of the seedlings were isolated and subjected for bisulfite treatment and library preparation. The resulting libraries were sequenced with Illumina sequencing technology.

first: Hsin-Yu

last: Hsieh

first: Ming-Ren

last: Yen

first: Chien-Chang

last: Wang

first: Yi-Jing

last: Lee

first: Shih-Long

last: Tu


title: Transcriptome of primary and metastatic human melanoma with silenced STAT3

city: Gdansk

first: Jakub

last: Mieczkowski

address: Debinki 12

country: Poland

institute: Medical University of Gdansk

summary: Primary and metastatic human melanoma cells were transfected with control siRNA or siSTAT3 to silence its expression. The global gene expression was evaluated after 48 h and related to gene levels in cells transfected with siRNA control.

overall_design:
Total RNAs were obtained, analyzed by micrarrays technology and differentially expressed, potentially STAT3 dependent genes were characterized.
STAT3 was silenced in patient-derived melanoma cells of different malignancy by using a specific siRNA and STAT3 dependent genes were identified

first: Bozena

last: Kaminska

first: Dorota

last: Kulesza

first: Kavita

last: Ramji


title: Innate and adaptive immunity cross-talk reprograms the tumor microenvironment to an inflammatory hub able to eliminate established poorly immunogenic tumors

city: Bethesda

middle: Joshua

last: Meyer

address: 41 Center Drive, Building 41, Room B620

department: National Cancer Institute

institute: National Institutes of Health

summary: Clinical benefit remains elusive for most patients with poorly inflamed carcinomas treated with immune checkpoint blockade. Alternative therapies able to convert the tumor microenvironment (TME) into a functionally inflamed immune hub may increase clinical benefit. Using comprehensive TME single-cell transcriptome, proteome, and immune cell analysis, we demonstrated that entinostat, a class I HDAC inhibitor, facilitates tumor deposition of the necrosis-targeted immunocytokine NHS-IL12 to promote potent anti-tumor efficacy against established MC38 and CT26 colon carcinoma models, with complete eradication of poorly immunogenic EMT6 breast tumors. Combination therapy reprogrammed the tumor innate and adaptive immunome to an inflamed landscape, where the concerted action of highly functional CD8+ T cells and activated neutrophils drove a dramatic macrophage M1-like polarization leading to complete tumor eradication. A biomarker signature of the mechanism involved in these studies is associated with patients’ overall survival in multiple tumor types. Collectively, these findings provide a rationale for combining NHS-IL12 with entinostat in the clinical setting.

overall_design: Single-cell RNAseq of immune cells in the tumor microenvironment enabled the identification of main immune subsets contributing to innate and adaptive cross-talk

first: Paul

last: Chariou

first: Sofia

last: Gameiro

first: Kristin

last: Hicks

first: Maggie

last: Cam

first: Jing

last: Bian

first: Jeffrey

last: Schlom


title: Differentially expressed genes of mRNAs between the TP53TG1-overexpressing Huh7 cells and its negative control

city: wuhan

first: Baiyang

last: Chen

address: donghu road 169

institute: wuhan university

summary: Hepatocellular carcinoma (HCC) is a cancer with global impact and largely refractory to current treatments. Novel treatment options are therefore urgently needed. LncRNAs play important regulatory roles in HCCs and are emerging as promising therapeutic options against HCC. We identified TP53TG1 as a promising tumor suppressor LncRNA. To understand TP53TG1 target genes and the mechanisms, we performed mRNA expression profiling in TP53TG1-overexpressing Huh7 cells and negative control.

overall_design: Huh7 cells were cultivated in vitro and transfection of TP53TG1 was performed in triplicate. Control was also processed in triplicate. And then they were subjected to gene expression profiling.

first: Jianwei

last: Lan

first: Yusha

last: Xiao

first: Pengpeng

last: Liu


title: Rare earth elements show antagonistic interactions as revealed by transcriptome profiling in Chlamydomonas reinhardtii.

city: Montreal

first: Elise

last: Morel

state: QC

address: 2900, boul. Édouard-Montpetit

department: Chemistry

country: Canada

institute: Univeristy of Montreal

summary:
Purpose; Here we compare the transcriptomic effects of three REEs; Ce, Tm and Y, and a mixture of all three on Chlamydomonas reinhardtii in order to determine the degree of overlap of their effects.
Methods; Transcriptome profiling (RNA-Seq) analysis performed on Chlamydomonas reinhardtii (wild-type strain, CC-125 aka 137c, Chlamydomonas resource center) exposed for 2 h to one of three soluble REEs (Ce, Tm, Y) salts at 0.5 μM or to an equimolar ternary mixture of these REEs. Illumina HiSeq (v.4) was used for the paired-end sequencing (2 × 100 base pairs) of 25 samples (5 replicates for each treatment: Ce; Tm; Y; Mix; Controls). For each sample, ca. 55 million of reads with their sequences, identification and quality scores were stored in two FastQ files.
Results; Known functions of the differentially expressed genes support effects of REEs on protein processing in the endoplasmic reticulum, phosphate transport and the homeostasis of Fe and Ca. The only stress response detected related to protein misfolding in the endoplasmic reticulum. When the REEs were applied as a mixture, antagonistic effects were overwhelmingly observed with transcriptomic results suggesting that the REEs were initially competing with each other for bio-uptake.
Conclusions; Our study represents the first detailed analysis of REE transcriptomic effects in a green microalga that is ubiquitous to fresh waters. Results generated by RNA-seq technology suggest that the approach of government agencies to regulate the REEs using biological effects data from single metal exposures may be a largely conservative approach.

overall_design: mRNA profiles of Chlamydomonas reinhardtii exposed for 2 h to one of three soluble REEs (Ce, Tm, Y) salts at 0.5 μM or to an equimolar ternary mixture of these REEs

first: Lei

last: Cui

first: William

last: Zerges

first: Kevin

last: Wilkinson


title: Regulating stem cell-related genes induces the plastic differentiation of cancer stem cells to treat cancer

status: Public on Jun 13 2021

city: Beijing

first: Jingying

last: Zhang

address: No. 38·, Xueyuan Road Haidian District

department: School of Pharmaceutical Sciences

institute: Peking University

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Single Cell Analysis of Mouse Lung Epcam+CD31/34/45- Epithelial Cells

city: Los Angeles

first: ting

last: Xie

address: 127 San Vicente Blvd

department: Pulmonary

institute: Cedars-Sinai Medical Center

summary: Epithelial cell homeostasis and renewal in the lung requires the supportive signals from surrounding mesenchymal cells. Single cell RNA-seq analysis was used to examine the gene expression levels of several receptors on the Sftpc+ alveolar type II stem cells. Single cell RNA-seq revealed Ghr, Cxcr2, Cxcr4, and Igf1r expressing cells were all Sftpc+ cells in the normal mouse lung.

overall_design: Stratification of lung epithelial subtypes in normal mouse.

first: Ting

first: Carol

last: Liang

last: Noble

first: Dianhua

last: Jiang


title: Transient genomic instability drives tumorigenesis through accelerated clonal evolution

city: La Jolla

first: Don

middle: W.

last: Cleveland

address: 9500 Gilman Drive

institute: Ludwig Institute for Cancer Research

summary: Abnormal numerical and structural chromosome content is frequently found in human cancer. However, the role of aneuploidy in tumor initiation and progression is poorly understood. To test the effect of aneuploidy on cancer development, we transiently induced chromosome instability (CIN) in mice by inducible overexpression of polo-like kinase 4 (PLK4), a master regulator of centrosome number. Short term increased PLK4 expression generated significant centrosome amplification and aneuploidy resulting in the formation of aggressive T cell lymphomas in mice with heterozygous inactivation of one p53 allele or accelerated tumor development in the absence of p53. Transient CIN increased the frequency of lymphoma-initiating cells, as revealed by T cell receptor sequencing of tumor samples. Transient CIN produced a unique tumor karyotype containing triploid chromosomes 4, 5, 14, and 15, as determined by whole genome sequencing.

overall_design: Examination of the effect of aneuploidy on tumor development.

first: Ofer

last: Shoshani


title: RNA-seq Analysis of BMDM treated with cancer-cell conditioned medium in the presence or abscence of lipid contents

city: Epalinges

first: Ping-Chih

last: Ho

state: Vaud

address: Ch. des Boveresses 155

department: Department of Fundamental Oncology

institute: University of Lausanne

summary: mRNA profiles of bone-marrow derived macrophages (BMDM) stimulated by cancer cell-conditioned medium in the presence or absnce of lipid contents

overall_design: The goals of this study are to use NGS to perform transcriptome profiling (RNA-seq) to find the transcriptome changes induced cancer cell-conditioned medium in the presence or absnce of lipid contents in bone-marrow derived macrophages (BMDM)

first: Giusy

last: Di Conza

first: Xin


title: Gene expression data from SKOV3 cell line with SND1 knockdown

city: Tianjin

first: Lingbiao

last: Xin

address: Qixiangtai RD 22

department: Biochemistry and Molecular Biology

institute: Tianjin Medical University

summary:
SND1 protein is a highly conserved protein of eukaryotic cells and is involved in a group of cellular biological processes, such as gene transcription, pre-mRNA splicing, cell cycle, DNA damage repair, proliferation and programmed cell death degradome, adipogenesis and cancerogenesis. SND1 can promote the metastasis and proliferation of breast cancer cells by down-regulating the miR-127 expression.
Herein, we used microarrays to detail the potential molecular mechanism in the ovarian cancer tumorigenesis.

overall_design: Total RNA were extracted in SKOV3 cells transfection with shSND1 and pLKO-Vector respectively. cDNA was synthesized and hybridised to Affymetrix microarrays.

first: Ran

last: Zhao

first: Jie

last: Yang


title: Next Generation Sequencing Facilitates Quantitative Analysis of Healthy Control and Patients of Systematic Lupus Erythematosus Neutrophil Transcriptomes

first: Xuan

address: dongdan

institute: Peking union medical college hospital

summary: We aimed to investigated the molecular mechanism of neutrophil in SLE. We isolated neutrophils from 6 new onset treatment-naïve SLE patients and 6 age/sex-matched HCs and examined the transcriptome by RNA-seq.

overall_design: Neutrophil lncRNA and mRNA profiles of healthy control and patients of systematic lupus erythematosus


title: Beauveria bassiana Glc8 (BbGlc8) regulating genes involved in conidiation

city: Hangzhou

first: Shenghua

last: Ying

state: Zhejiang

address: Yu-hang-tang Road 688

institute: Zhejiang University

summary: Gene BbGlc8 playes an essential role in conidation, a determinant to the biocontrol  potential of entomopathogenic fungi.  The genome-wide exprssion analysis involved in fungal conidiation was analyzed by using high throughput sequencing (RNA-Seq). Our transcriptional profiles revealed that numerous differentially expressed genes (DEGs), of which involved in metabolism, cell transport and cell rescue, were significantly involved in deveopment of fungal conida.

overall_design: Total RNA obtained from ∆BbGlc8 disruption mutant were compared to that of wild type strain (WT) grown on SDA plates (Glucose 4%, Peptone 1%, and Yeast extract 1% plus 1.5% Agar).

first: Sheng-Hua

first: Ming-Guang

last: Feng


title: Regulating stem cell-related genes induces the plastic differentiation of cancer stem cells to treat cancer [in vitro]

first: Jingying

summary: Relapse of cancer is associated with multi-directional differentiation, and unrestricted proliferative replication potential of cancer stem cells. Herein, we propose the plastic differentiation strategy for irreversible differentiation of cancer stem cells. Whole gene expression analysis revealed that salinomycin induced the cancer stem cells into normal cells, dormant cells, and mature cancer cells. Besides, the results indicated that the gatekeeper was related to the inhibition of PKC α signaling pathway. The differentiated normal or dormant cells were incorporated into normal tissue, while the rest were killed by chemotherapy. Our findings would offer the evidence for plastic differentiation of cancer stem cells, and propose an invert strategy for cancer therapy.

overall_design: 3 samples

first: Qian

last: Luo

first: Jiarui

last: Xu

first: Jing

last: Bai

first: Limin

last: Mu

first: Yan

last: Yan

first: Jialun

last: Duan

first: Yinuo

last: Cui

first: Zhanbo

last: Su

first: Ying

first: Wanliang

last: Lu


title: Time-lapse super-resolution imaging reveals key principles for cis-limited Xist RNA localization [ChrRNA-seq]

status: Public on Jun 12 2021

city: Oxford

first: Guifeng

last: Wei

address: South Parks Road

department: Department of Biochemistry

country: United Kingdom

institute: University of Oxford

summary: Xist RNA, which directs the process of X chromosome inactivation in mammals, localizes in cis over the chromosome from which it is transcribed, recruiting chromatin modifiers to silence underlying genes.  To analyze cis-limited Xist RNA localization we have developed time-resolved super-resolution imaging of individual Xist RNA molecules in single cells. Using this approach, we quantify fundamental parameters underpinning Xist RNA dynamics, demonstrating a feedback mechanism linking Xist RNA synthesis and degradation, and an unusual coupling behavior that physically links temporally separated Xist RNA molecules. Additionally, we show that the protein SPEN, a key factor for Xist-mediated gene-silencing, has a separable function in Xist RNA localization, stability and in coupling behavior. Our results provide important insights towards understanding the unique and unusual behavior of Xist RNA.

overall_design: We isolated chromatin-associated RNA (ChrRNA) to analyze the allelic ratio, aiming to understand Xist-mediated Silencing. Xist RNA is labeled.The ChrRNA was isolated from cells with trangenic Xist model (iXist-Chr15) or endogenous Xist model (iXist-ChrX) derived from mouse embryonic stem cells. Cell lines with different factor knockout (CIZ1, SpenRRM, SpenSPOCmut) were generated. The allelic ratios were systematically and comprehensively compared.

first: L

last: Rodermund

first: H

last: Coker

first: G

first: N

last: Brockdorff


title: Transcriptomic and epigenomic profiling of young and aged spermatogonial stem cells reveals molecular targets regulating differentiation

city: Hong Kong

first: Jinyue

last: Liao

address: Room 38016, 1/F Lui Che Woo Clinical Sciences Building

department: Department of Chemical Pathology

country: Hong Kong

institute: The Chinese University of Hong Kong