title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR509YOX)

summary:
H3K27me3 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: Control Mint-ChIP-seq from T-helper 17 cell (ENCSR104DYP)

status: Public on Jul 22 2022

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

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: TF ChIP-seq from K562 (ENCSR103TYK)

summary:
eGFP-HBP1 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 ChIP-seq from middle frontal area 46 (ENCSR105CRB)

summary:
Control ChIP-seq on middle frontal area 46 tissue male adult (90 or above years) with mild cognitive impairment.

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: Histone ChIP-seq from ovary (ENCSR509SNH)


title: Control ChIP-seq from SK-N-SH (ENCSR921JGF)

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 HCT116 (ENCSR108CCH)


title: Mint-ChIP-seq from HCT116 (ENCSR510LJL)


title: Mint-ChIP-seq from HCT116 (ENCSR324ZNP)


title: TF ChIP-seq from heart right ventricle (ENCSR105KGD)


title: Control Mint-ChIP-seq from HCT116 (ENCSR508TCS)


title: Mint-ChIP-seq from HCT116 (ENCSR324QIZ)


title: Mint-ChIP-seq from natural killer cell (ENCSR326YSR)


title: Mint-ChIP-seq from natural killer cell (ENCSR326JGI)


title: Mint-ChIP-seq from HCT116 (ENCSR919YMZ)


title: Control ChIP-seq from GM12878 (ENCSR919BBP)

summary:
GM12878 immortalized cell line stably expressing C-terminal eGFP-ZBTB4 fusion protein.

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 placenta (ENCSR918ESG)


title: TF ChIP-seq from K562 (ENCSR506SSQ)

summary:
ZNF354C 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 ChIP-seq from K562 (ENCSR316UUM)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-TBPL1 fusion protein.

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 H1 (ENCSR704AQC)


title: Mint-ChIP-seq from effector memory CD8-positive, alpha-beta T cell (ENCSR707ZDY)


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR507SXH)


title: TF ChIP-seq from middle frontal area 46 (ENCSR705DNM)

summary:
CTCF ChIP-seq on middle frontal area 46 tissue female adult (90 or above 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 central memory CD8-positive, alpha-beta T cell (ENCSR919UYS)


title: Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR322MTA)


title: Control Mint-ChIP-seq from HCT116 (ENCSR704TRV)


title: Mint-ChIP-seq from nephron (ENCSR103RLW)

summary:
H3K27me3 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: Control ChIP-seq from activated CD8-positive, alpha-beta T cell (ENCSR314QKF)


title: Mint-ChIP-seq from IgD-negative memory B cell (ENCSR915ISE)


title: Mint-ChIP-seq from HCT116 (ENCSR323XBZ)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR703AIO)


title: Control Mint-ChIP-seq from central memory CD8-positive, alpha-beta T cell (ENCSR308NMT)


title: Mint-ChIP-seq from HCT116 (ENCSR314MXA)


title: TF ChIP-seq from K562 (ENCSR307YJU)

summary:
eGFP-MYNN 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 T-cell (ENCSR912FCF)


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR317QET)


title: Control ChIP-seq from right lobe of liver (ENCSR309LQG)


title: Control ChIP-seq from K562 (ENCSR506DBU)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-MLX fusion protein.

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 HCT116 (ENCSR910OOE)


title: Mint-ChIP-seq from activated naive CD4-positive, alpha-beta T cell (ENCSR103OSN)


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR505DQN)


title: Control ChIP-seq from K562 (ENCSR504LIP)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-ZNF57 fusion protein.

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 HCT116 (ENCSR906ZFR)


title: Mint-ChIP-seq from HCT116 (ENCSR702AWL)


title: Mint-ChIP-seq from CD14-positive monocyte (ENCSR905UNZ)

summary:
H3K4me3 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: TF ChIP-seq from K562 (ENCSR504HOI)

summary:
eGFP-SRF 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: TF ChIP-seq from SK-N-SH (ENCSR701SED)

summary:
eGFP-OSR1 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 immature natural killer cell (ENCSR102BZX)

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: Control ChIP-seq from middle frontal area 46 (ENCSR103IXF)


title: Mint-ChIP-seq from natural killer cell (ENCSR701GXD)


title: Mint-ChIP-seq from T-helper 17 cell (ENCSR103GBF)


title: TF ChIP-seq from HepG2 (ENCSR903JFF)

summary:
ChIP-Seq on HepG2

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 CD8-positive, alpha-beta T cell (ENCSR701JGD)

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: Histone ChIP-seq from heart left ventricle (ENCSR300WWL)

summary:
H3K4me3 ChIP-seq on heart left ventricle tissue male adult (54 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 CD4-positive, alpha-beta T cell (ENCSR101QKW)


title: TF ChIP-seq from HepG2 (ENCSR905BNO)


title: TF ChIP-seq from K562 (ENCSR303SHG)

summary:
eGFP-ZNF699 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 HCT116 (ENCSR099TYF)


title: Control Mint-ChIP-seq from HCT116 (ENCSR500IKB)


title: Histone ChIP-seq from heart right ventricle (ENCSR501GLO)

summary:
H3K4me1 ChIP-seq on heart right ventricle tissue male adult (66 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 (ENCSR099ETQ)

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 HCT116 (ENCSR098CPV)


title: IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

city: Hershey

first: Aron

last: Lukacher

state: PA

address: 500 University Dr.

department: Microbiology & Immunology

institute: Penn State College of Medicine

type: Expression profiling by high throughput sequencing

summary: To investigate the effect of interleukin (IL)-21 signaling on CD8 T cells and compare IL21-receptor deficient CD8 T cells to CD8 T cells derived from CD4 T cell deficient mice, we infected IL21-receptor knock-out mice, CD4 T cell depleted mice, and wild-type mice intracranially with Mouse Polyomavirus. We then performed gene expression profiling analysis using data obtained from RNA-seq of CD8 T cells derived from the brains of the mice at 30 day post infection.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for CD8 T cells derived from the brains of IL21-receptor knock-out mice, CD4 T cell deficient mice, or wildtype mice at 30 day post Mouse Polyomavirus infection (dpi).

first: Heather

last: Ren

first: Mingqiang


title: RNA sequencing reveals the expression profiles of long noncoding RNA in lipopolysaccharide-induced sepsis

city: Beijing

first: Haiyan

last: Liao

state: Beijing

address: 168 Litang Road Changping District, Beijing, China

country: China

institute: Tsinghua University

summary:
There are currently no specific diagnostic biomarkers and effective pharmacological treatments for sepsis, which makes the mortality rate remains high. Although non-coding RNAs seem to be superior candidates as biomarkers and therapeutics for sepsis, the role of long noncoding RNA (lncRNA) in sepsis remains not completely understood.
We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells at the same time point.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for lipopolysaccharide (LPS) induced sepsis  human umbilical vein endothelial cells (HUVECs)  and normal HUVECs.


title: Lactobacillus reuteri normalizes altered fear memory in CNTNAP4 knockout mouse (male)

city: Guangzhou

first: Wenlong

last: Zhang

address: Yuexiu

institute: The First Affiliated Hospital of Guangzhou Medical University

summary: To explore function that CNTNAP4 in the regulation of GABAergic transmission,, we profiled basolateral amygdala from wild-type and CNTNAP4 knockout in male mice by RNA sequencing (RNA-seq).

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of WT and CNTNAP4-/- mice

first: Jie

last: Huang

first: Feng

last: Gao

first: Yunlong


title: Mint-ChIP-seq from CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR093VUP)


title: Mint-ChIP-seq from HCT116 (ENCSR088ZGM)


title: Control ChIP-seq from SK-N-SH (ENCSR094JSJ)

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 naive B cell (ENCSR077XOM)


title: TF ChIP-seq from B cell (ENCSR075NRV)


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR081XLT)


title: Control ChIP-seq from K562 (ENCSR093QJW)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-RAD21 fusion protein.

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 (ENCSR082DLA)


title: Mint-ChIP-seq from T-helper 17 cell (ENCSR079EXG)


title: TF ChIP-seq from K562 (ENCSR077TKJ)

summary:
eGFP-ZNF707 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 stimulated activated effector memory CD8-positive, alpha-beta T cell (ENCSR072ORU)


title: TF ChIP-seq from WTC11 (ENCSR096OUP)

summary:
eGFP-NFATC4 ChIP-seq on human WTC11

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 HCT116 (ENCSR071RJS)


title: Mint-ChIP-seq from T-cell (ENCSR073ORI)


title: Mint-ChIP-seq from HCT116 (ENCSR070KNB)


title: Mint-ChIP-seq from activated T-helper 1 cell (ENCSR068YVZ)

summary:
H3K27me3 Mint-ChIP-seq on activated T-helper 1 cell male adult (35 years) treated with 1 ug/mL Interleukin-4 antibody , 30 ng/mL Interleukin-12 subunit alpha , 30 ng/mL Interleukin-12 subunit beta , 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 naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR070AET)


title: TF ChIP-seq from middle frontal area 46 (ENCSR068DJS)

summary:
CTCF ChIP-seq on middle frontal area 46 tissue male adult (90 or above years) with mild cognitive impairment

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 T-cell (ENCSR068BIF)


title: Mint-ChIP-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR065UTP)

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 central memory CD8-positive, alpha-beta T cell (ENCSR061PIA)


title: TF ChIP-seq from HepG2 (ENCSR066EWR)


title: Mint-ChIP-seq from natural killer cell (ENCSR067KOO)


title: Control ChIP-seq from K562 (ENCSR065HVA)


title: Histone ChIP-seq from heart left ventricle (ENCSR066SQU)

summary:
H3K27me3 ChIP-seq on heart left ventricle tissue male adult (54 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 HCT116 (ENCSR065OMZ)


title: Histone ChIP-seq from ovary (ENCSR061IAQ)


title: Histone ChIP-seq from E14TG2a.4 (ENCSR059MBO)

summary:
PSU mouse E14Tg2a.4 H3K27me3 ChIP-seq

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 stimulated activated memory B cell (ENCSR053RFF)

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 effector memory CD8-positive, alpha-beta T cell (ENCSR055TVU)


title: Control Mint-ChIP-seq from naive B cell (ENCSR056PPJ)


title: Mint-ChIP-seq from dendritic cell (ENCSR047WCC)


title: Control ChIP-seq from MCF-7 (ENCSR044HDZ)

summary:
MCF7 immortalized cell line stably expressing C-terminal eGFP-SRF fusion protein.

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 MCF 10A (ENCSR049WGG)


title: Mint-ChIP-seq from effector memory CD8-positive, alpha-beta T cell (ENCSR049YHC)


title: Mint-ChIP-seq from CD4-positive, alpha-beta memory T cell (ENCSR041YWB)

summary:
H3K27ac 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: TF ChIP-seq from K562 (ENCSR041QAZ)

summary:
RNF219 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 B cell (ENCSR040ZML)


title: Mint-ChIP-seq from central memory CD8-positive, alpha-beta T cell (ENCSR040TXN)


title: TF ChIP-seq from mucosa of descending colon (ENCSR038VWU)

summary:
CTCF ChIP-seq on mucosa of descending colon tissue male adult (40 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 CD4-positive, alpha-beta T cell (ENCSR038NSJ)


title: Control ChIP-seq from HepG2 (ENCSR032BUQ)

summary:
HepG2 immortalized cell line stably expressing C-terminal eGFP-RAD21 fusion protein.

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 (ENCSR041JSH)

summary:
H3K27me3 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 activated naive CD8-positive, alpha-beta T cell (ENCSR036DBU)


title: Mint-ChIP-seq from natural killer cell (ENCSR035FAV)


title: Mint-ChIP-seq from stimulated activated naive CD8-positive, alpha-beta T cell (ENCSR033WMA)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR036OBW)

summary:
H3K27me3 ChIP-seq on middle frontal area 46 tissue male adult (90 or above years) with mild cognitive impairment

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 (ENCSR029KZF)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-MAZ fusion protein.

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 natural killer cell (ENCSR025UNZ)


title: Mint-ChIP-seq from stimulated activated naive CD8-positive, alpha-beta T cell (ENCSR030KTV)


title: TF ChIP-seq from K562 (ENCSR026RAK)

summary:
eGFP-MXD1 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 CD14-positive monocyte (ENCSR707HMU)

summary:
H3K27me3 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 activated T-cell (ENCSR022SNQ)


title: Control ChIP-seq from middle frontal area 46 (ENCSR018KWK)


title: TF ChIP-seq from WTC11 (ENCSR023IPQ)

summary:
eGFP-PRRX2 ChIP-seq on human WTC11

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 central memory CD8-positive, alpha-beta T cell (ENCSR016WNP)


title: Mint-ChIP-seq from H9 (ENCSR016RFN)

summary:
H3K27me3 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 ChIP-seq from MCF 10A (ENCSR011HCN)


title: TF ChIP-seq from HepG2 (ENCSR015LYB)

summary:
ChIP-Seq on HepG2

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 (ENCSR015BRP)

summary:
K562 immortalized cell line stably expressing C-terminal eGFP-ZNF695 fusion protein.

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 naive CD4-positive, alpha-beta T cell (ENCSR007JEX)


title: Mint-ChIP-seq from dendritic cell (ENCSR015IZP)


title: Mint-ChIP-seq from activated T-cell (ENCSR006QLV)


title: Control ChIP-seq from activated B cell (ENCSR003FJP)


title: Control ChIP-seq from SK-N-SH (ENCSR000SND)

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: Histone ChIP-seq from heart left ventricle (ENCSR017LLJ)

summary:
H3K36me3 ChIP-seq on heart left ventricle tissue female adult (56 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: RNA-sequencing data of TIP60 mutated and control HEK293 cells

city: Parkville

first: Alexandra

last: Garnham

state: Victoria

address: 1G Royal Parade

country: Australia

institute: Walter and Eliza Hall Institute of Medical Research

summary: In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to HEK293 cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on HEK293 cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 3 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.

overall_design: RNA-sequencing data was generated for 8 samples of human embryonic kidney cells 293 (HEK293). Of these samples, 4 are control and 4 are TIP60 knock-out (KO). Differential analyses were performed, identifying differentially expressed genes between the KO and control groups.

middle: L

first: Johannes

last: Wichmann

first: Anne

last: Voss


title: RNA-sequencing data of TIP60 mutated and control U2OS cells

summary: In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to U2OS cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on U2OS cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 4 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.

overall_design: RNA-sequencing data was generated on 11 samples of human U2OS cells which are either control or TIP60 knock-out (KO). All samples have drosophila melanogaser S2 cells spiked in for normalization purposes. Differentially analyses were carried out between the control and KO groups.


title: TF ChIP-seq from right lobe of liver (ENCSR000VGD)

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: Identification of the circadian clock genes as components of the compensatory mechanism in nphp8 mutant zebrafish

city: Freiburg im Breisgau

first: Toma

middle: Antonov

last: Yakulov

address: Hugstetter Str. 55

department: Department of Medicine

country: Germany

institute: University Freiburg Medical Center

summary: The nphp8sa24730 mutant zebrafish displayed a marked decrease in glomerular cysts and cloaca malformation over subsequent generations, implying the existence and activation of compensatory mechanisms that could rescue the ciliopathy-associated phenotypes. To uncover these mechanisms, we compared the transcriptional profiles of two-day-old maternal zygotic homozygous nphp8sa24730 mutant larvae and control siblings by RNA sequencing (RNA-seq).

overall_design: Comparative gene expression profiling analysis of RNA-seq data for two-day-old maternal zygotic homozygous nphp8(sa24730) mutant zebrafish larvae and control siblings.

first: Friedemann

last: Zaiser

first: Anna

middle: C

last: Veenstra

first: Hui

last: Wang

first: Burulca

last: Göcmen

first: Priska

last: Eckert

first: Henriette

last: Franz

last: Köttgen

first: Gerd

last: Walz

middle: A


title: Detection of H2AZ acetylation, total H2AZ, and H4K8 and H4K16 acetylation by CUT&Tag-sequencing

summary: In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to U2OS cells. CUT&Tag was performed on replicate cultures and 100,000 cells per sample, 43,000 human cells each of U2OS with inducible single guide RNA #1 (g1/C9) or  inducible single guide RNA #2 (g2/C9) expression and both with constitutive expression of Cas9 enzyme, either treated with doxycycline for 4 days (KO) or untreated (CTL) and 57,000 D. melanogaster cells as a spike-in, in total two replicates of TIP60 deleted cells and two replicates of control cells.

overall_design: CUT&Tag-sequencing data were generated on 22 samples of human U2OS cells which are either control (CTL) or TIP60 knock-out (KO) using antibodies to H2AZK4_7_11ac, H2AZK4_7ac, total H2AZ,  H4K8ac, H4K16ac, a positive control (H3K27me3) and a negative control (IgG). All samples have Drosophila melanogaser S2 cells spiked in for normalization purposes. Differentially analyses were carried out between the control and KO groups within antibody.


title: Mint-ChIP-seq from stimulated activated effector memory CD8-positive, alpha-beta T cell (ENCSR004YPL)

first: ENCODE

last: DCC


title: TIP60 mutant and control RNA-seq and CUTandTag-seq data

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Mint-ChIP-seq from naive B cell (ENCSR024NBY)


title: PLTP is a p53 target gene with roles in cancer growth suppression and ferroptosis

city: Philadelphia

first: Priyankara

middle: J

last: Wickramasinghe

address: 3601 Spruce Street

department: Bioinformatics

institute: The Wistar Institute

summary: The tumor suppressor protein p53 suppresses cancer by regulating processes such as apoptosis, cell cycle arrest, senescence, and ferroptosis.  Whereas numerous p53 target genes have been identified, only a few appear to be critical for the suppression of tumor growth.  Additionally, while ferroptosis is clearly implicated in tumor suppression by p53, few p53 target genes with roles in ferroptosis have been identified.  We have been studying the activity of germline missense variants of p53 that are hypomorphic.  These hypomorphic variants are associated with increased risk for cancer, but they retain the majority of p53 transcriptional function; as such, study of the transcriptional targets of these hypomorphs has the potential to reveal genes that are important for p53-mediated tumor suppression.  Here, we identify PLTP (phospholipid transfer protein) as a p53 target gene that shows impaired transactivation by three different cancer-associated p53 hypomorphs: P47S (Pro47Ser, rs1800371), Y107H (Tyr107His, rs368771578), and G334R (Gly334Arg, rs78378222).  We show that enforced expression of PLTP potently suppresses colony formation in human tumor cell lines.  We also show that PLTP regulates the sensitivity of cells to ferroptosis, which is an iron mediated and lipid peroxide-induced cell death pathway.  Taken together, our findings reveal PLTP to be a p53 target gene that is extremely sensitive to p53 transcriptional function, and which has roles in growth suppression and ferroptosis

overall_design: RNA-seq analysis of LCL cells with WT and P47S p53 variant treated with nutlin

first: Keerthana

last: Gnanapradeepan

first: Maureen

last: Murphy


title: Macrophage proliferation machinery leads to PDAC progression, but susceptibility to innate immunotherapy.

city: St. Louis

first: Chong

last: Zuo

address: 4559 Scott Ave

institute: Washington University in Saint Louis

summary: Tumor-associated macrophages (TAMs) are involved in many aspects of cancer progression and correlated with poor clinical outcomes in many cancer types, including pancreatic ductal adenocarcinomas (PDACs). Previous studies have shown that TAMs can populate PDAC tumors not only by monocyte recruitment but also by local proliferation. However, the impact local proliferation might have on macrhopage phenotype and cancer progression is unknown.  Here, we utilized genetically engineered cancer models, single-cell RNA-sequencing data, and in vitro system to show that proliferation of TAMs was driven by colony stimulating factor-1 (CSF1) produced by cancer-associated fibroblasts. CSF1 induced high levels of p21 in macrophages, which regulated both TAM proliferation and phenotype. TAMs in human and mouse PDACs with high levels of p21 had more inflammatory and immunosuppressive phenotypes, independent of their proliferative status. The p21 expression in TAMs was induced by both stromal interaction and/or chemotherapy treatment. Finally, by modeling p21 expression levels in TAMs, we found that p21-driven macrophage immunosuppression in vivo drove tumor progression. Serendipitously, the same p21-driven pathways that drive tumor progression, also drive response to CD40 agonist. These data suggest that stromal or therapy-induced regulation of cell cycle machinery can regulate both macrophage-mediated immune suppression and susceptibility to innate immunotherapy.

overall_design: Examination of macrophage subsets in steady-state and PDAC tissue and after chemotherapy treatments


title: TF ChIP-seq from SK-N-SH (ENCSR008LHT)

summary:
eGFP-ISL1 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: Erythroblastic islands foster granulopoiesis in parallel to terminal erythropoiesis

city: Cincinnati

first: Nathan

last: Salomonis

state: OH

address: 3333 Burnet Avenue

department: Biomedical Informatics

institute: Cincinnati Children's Hospital

summary: The erythroblastic island (EBI), composed of a central macrophage and surrounding maturing erythroblasts, is the erythroid precursor niche.  Despite numerous studies, its precise composition is still unclear. Using multispectral imaging flow cytometry (IFC), in vitro island reconstitution, and single cell RNA-seq of EBI-component cells enriched by gradient sedimentation, we present evidence that CD11b+ cells present in the EBIs are neutrophil precursors specifically associated with bone marrow EBI macrophages, indicating that erythro-(myelo)-blastic islands are a site for terminal granulopoiesis as well as erythropoiesis and production of these lineages is dynamically regulated within this niche.  We further demonstrate that the balance between these lineages is determined by pathophysiological conditions, favoring granulopoiesis during anemia of inflammation, or erythropoiesis after erythropoietin (Epo) stimulation.  Finally, we provide the heterogeneous molecular profiling of EBI macrophages as revealed by Cellular Indexing of Transcriptome and Epitopes (CITE)-sequencing of mouse bone marrow EBIs at baseline and after Epo-stimulation in vivo.  Altogether, these data demonstrate that EBIs serve a dual role as terminal erythropoiesis and granulopoiesis niches and the central macrophages adapt to the needs of stress erythropoiesis as well as granulopoiesis.

overall_design: Single-cell RNA-Seq and CITE-Seq of murine erythroblastic islands

first: Katie

middle: G

last: Seu

first: Laurel

last: Romano

first: Julien

last: Papoin

first: Edward

middle: D

last: Muench

first: Diamantis

last: Konstantinidis

first: André

last: Olsson

first: Katrina

last: Schlum

first: Kashish

last: Chetal

first: Joel

last: Chasis

first: Mohandas

last: Narla

first: Betsy

last: Barnes

first: Yi

last: Zheng

first: H

last: Grimes

first: Lionel

last: Blanc

first: Theodosia

last: Kalfa


title: The interweaved signatures of common-gamma-chain cytokines across immunologic lineages

city: Boston

first: Liang

last: Yang

state: MA

address: 77 Avenue Louis Pasteur

department: Pathology

institute: Harvard Medical School

summary: "γc" cytokines are a family whose receptors share a “common gamma chain” signaling moiety, and play central roles in the differentiation, homeostasis and communications of all immunocyte lineages. As a resource to better understand their range and specificity of action, we profiled by RNAseq the immediate-early responses to the main γc cytokines, across all immunocyte lineages. The results show a different response landscape than expected: broader, with a strong Myc-controlled resetting of biosynthetic and metabolic pathways, a major downregulation component, and extensive overlap between cytokines (one cytokine doing in one cell what another does elsewhere). Various mechanisms appear involved: fast transcriptional activation, chromatin remodeling, and mRNA destabilization. Other surprises are uncovered: IL2 effects in mast cells, major shifts between follicular and marginal-zone B cells, paradoxical and cell-specific cross-talk between IFN and γc signaling, or an NK-T like program induced by IL21 in CD8+ T cells.

overall_design: Two replicates of follicular B cell samples, PBS-treated control and IL4-treated, underwent CUT&RUN to analyze the following targets: IgG, H3K4me1, H3K4me3, H3K27me3, H3K36me3, H3K27ac, and H3.3.

first: Alev

last: Baysoy

first: Kumba

last: Seddu

first: Tamara

last: Salloum

first: Caleb

last: Dawson

first: Juliana

last: Lee

first: Shani

last: Gal-Oz

first: Hadas

last: Ner-Gaon

first: Julie

last: Tellier

first: Alberto

last: Millan

first: Alexander

last: Sasse

first: Brian

last: Brown

first: Lewis

last: Lanier

first: Tal

last: Shay

first: Stephen

last: Nutt

first: Daniel

last: Dwyer

first: Christophe

last: Benoist


title: Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR002YXM)

first: ENCODE

last: DCC


title: Seq-Scope analysis of human acne

city: Ann Arbor

first: Jun Hee

state: MI

address: 109 Zina Pitcher Pl

institute: University of Michigan

summary: Skin samples were analyzed through Seq-Scope.

sample_organism:
Homo sapiens
synthetic construct

platform_organism:
Homo sapiens
synthetic construct

overall_design: A 6 mm punch skin biopsy was frozen in OCT medium and stored at -80°C until sectioning. The current study utilized Seq-Scope[HISEQ], which is similar to the previously described version of Seq-Scope [MISEQ] (PMID: 34115981), but utilized the HISEQ2500 flow cells for Seq-Scope array generation, instead of the MISEQ flow cells. All the procedures are extensively described in the former paper, and current study was performed almost identically; however, following things were different between the two studies: (1) To perform the 1st-Seq process, HISEQ2500 sequencing was performed with 100 pM of HDMI32-oligo library, and generated 1.1 million clusters/mm^2 fully sequenced pixel density (PF clusters). (2) HISEQ2500 tiles have a rectangular shape and are arranged to form a minimally interrupted large imaging area. Therefore, images from individual tiles were assembled to present a larger image that can be aligned with the hematoxylin and eosin histology results. (3) To accommodate the larger imaging area, volume of the solutions was proportionally increased during the experiment. (4) During the secondary strand synthesis, we used an updated Randomer sequence (5’-TCAGACGTGTGCTCTTCCGATCTNNNNNNNNB-3’). Compared to the original Randomer (5’-TCAGACGTGTGCTCTTCCGATCTNNNNNNNNN-3’), the updated Randomer sequence does not anneal to the poly-A region, enabling more efficient transcriptome alignment. (5) To further substantiate our former results from scRNA-seq and spatial-seq, we focused on one acne sample, which presented an ideal spatial orientation that reveals the relationship between diverse inflammatory populations (including TREM2 macrophages) and hair follicle pathology. Other experimental details and analysis methods are as described in the previous study.

first: Jer-En

last: Hsu

first: Chun-Seok

last: Cho

first: Myungjin

last: Kim

first: Jingyue

last: Xi

first: Johann

middle: E

last: Gudjonsson


title: RNA-sequencing data of Tip60 deleted and control mouse embryonic fibrobasts

first: Alexandra

last: Garnham

summary: In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to MEFs. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on MEFs, where the TIP60 gene was deleted using Cre/loxP technology. Nuclear translocation was induced with 4-OH-tamoxifen treatment for 3 and 5 days to induce TIP60 gene deletion in the samples also containing the loxP sited in the Tip60 locus.

overall_design: RNA-sequencing data was generated for 14 mouse embryonic fibroblast samples. These samples are either control or Tip60 knock-out (KO), that have been treated for either 3 or 5 days to induce Tip60 KO. Differential analyses were undertaken to identify differential genes between KO and control groups at both 3 and 5 days.

first: Johannes

last: Wichmann

first: Anne

last: Voss


title: Mint-ChIP-seq from brain (ENCSR000FYV)

summary:
H3K4me1 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: Lactobacillus reuteri normalizes altered fear memory in CNTNAP4 knockout mouse

status: Public on Jul 21 2022

first: Wenlong

last: Zhang

summary: To explore the function of CNTNAP4 in the regulation of GABAergic transmission, we profiled basolateral amygdala from wild-type and CNTNAP4 knockout female mice by RNA sequencing (RNA-seq).

overall_design: We performed gene expression profiling analysis using data obtained from RNA-seq of WT and CNTNAP4-/- mice

first: Jie

last: Huang

first: Feng

last: Gao

first: Yunlong


title: Microenvironmental Bmp4 inhibits post-irradiation regenerative response of the salivary gland

city: Groningen

first: Rob

last: Coppes

address: Ant. Deusinglaan 1

department: Biomedical Sciences of Cells and Systems

country: Netherlands

institute: University Medical Center Groningen

summary: Radiotherapy of head and neck cancer is accompanied by unavoidable co-irradiation of the salivary gland, often resulting in hyposalivation and reduced quality of life. Irradiated salivary gland tissue is characterized by the presence of cellular senescence, fibrosis, and a chronic inflammatory state changing the cellular microenvironment. These microenvironmental changes may be unfavorable for the regenerative potential of tissue stem cells inhibiting regenerative medicine options. Therefore, we investigated microenvironmental changes of the irradiated murine salivary gland and their effect on the potency of salivary gland stem/progenitor cells (SGSCs). After 15 Gy local irradiation of murine salivary glands, alongside an in time advancing decline in function, the submandibular gland (SMG) showed extensive fibrosis, p21-expressing senescent cells, and immune cell infiltration, all indicative of microenvironmental changes. Additionally, irradiated SMG contained a lower number of CD24++/CD29++ and CD24++/CD29+ stem/progenitor cell enrichment marker-expressing cells 30 days post-irradiation which coincides with a reduction in salisphere formation potential over time. However, after subsequent passaging of organoids derived from glands obtained 14 days after irradiation, and to a lesser extent at 30 days post-irradiation, the ability to form secondary organoids recovered to control levels. In contrast, cells obtained from glands at 90, 180, and 360 days post-irradiation irreversibly lost their ability to form organoids, indicating a time-dependent loss of regenerative potential. Transcriptomic analysis showed overexpression of Bmp4 in day 90 organoids derived from irradiated glands compared to the ones from day 14. Inhibition of Bmp4 using Noggin reversed this adverse response suggesting an important role in modulating SGSC function. Thus, early after irradiation, the regenerative potential of surviving SGSCs is preserved and comparable to that of unirradiated cells. At later time points after irradiation, SGSCs lose their regenerative potential suggesting that the prolonged exposure to a deleterious microenvironment leads to an irreversible decline in stemness. Modulation of Bmp4 signaling pathway might improve the regenerative potential of surviving SGSCs and enhance the efficiency of stem cell therapy in restoring the functionality of irradiated salivary glands.

overall_design: Examination of passage 1 and passage 2 organoids derived from salivary glands at 14 and 90 days post (sham) IR

middle: P


title: The gene transcription of the efficient biodetoxification filamentous fungus Amorphotheca resinae ZN1 against the model lignocellulosic inhibitors

city: Changzhou

first: Xia

last: Yi

address: Gehu Middle Road #21

institute: Changzhou University

summary: Furans (furfural and 5-hydroxymethylfurfural (HMF)), phenolic aldehydes (4-hydroxybenzaldehyde, syringaldehyde, and vanillin), and weak acids (acetic acid and formic acid) are the main degradation products of lignocellulose pretreatment process and seriously inhibit the cellullas enzyme activity and the fermentation process.

overall_design: To investigate the gene transcription profiling of A. resinae ZN1 against the model lignocellulosic inhibitors, we carried out transcriptomic sequencing assays.

last: Bao

first: Qiuqiang

last: Wang

first: Xiaochuang


title: Hedgehog Induced ZFYVE21 Activates T Cell Intrinsic, NLRP3 Inflammasomes to Promote Chronic Inflammation

city: New Haven

first: Shaoxun

state: CT

address: 11 Dixwell Ave, Apt 212

institute: Yale University

summary: ZFYVE21 is a novel Rab5 effector involved in immune signaling whose functions in vivo are undefined. Using humanized mouse models and patient specimens, we describe a T cell-autonomous role for ZFYVE21 in promoting chronic inflammation. Following ischemia reperfusion injury (IRI), endothelial cells (ECs) produce Hedgehog (Hh) ligands. Hh ligands induce expression of ZFYVE21 in a “Ptchhi” cell population (CD3+CD4+CD45RO+Ptch1hiPD-1hi) that is highly responsive to Hh signaling and which display vigorous EC-mediated recruitment and effector responses in vivo. Mechanistically, following IFN-gamma-dependent priming, Hh-induced ZFYVE21 modulates T cell intrinsic, NLRP3 inflammasome activity in an Akt-dependent manner to allow IL-18-mediated potentiation of IFN-gamma responses. Hh-induced NLRP3 inflammasomes and T cell-specific ZFYVE21 augment vascular sequelae of chronic inflammation. Moreover, Ptchhi T cells highly expressing ZFYVE21 are expanded in IRI patients, and frequencies of these cells are modulated by Hh signaling. Hh-induced ZFYVE21 activates T cell intrinsic, NLRP3 inflammasomes to promote chronic inflammation.

overall_design: To do this, Tmem from 4 donors were stimulated with anti-CD3 in the presence of either anti-CD28 or SAG, and the P1-P4 populations emerging from these treatments were FACS-sorted for RNA sequencing.

first: Bo

last: Jiang

first: Song

last: Guiyu

first: Quan

first: Matthew

last: Fan

first: Caodi

last: Fang

first: Xue

last: Li

first: Chien

last: Soh

first: Thomas

last: Manes

first: Nardos

last: Cheru

first: Lingfeng

last: Qin

first: Pengwei

last: Ren

first: Bianca

last: Jortner

first: Emma

last: Quaranta

first: Peter

last: Yoo

first: Arnar

last: Geirsson

first: Robert

last: Davis

first: George

last: Tellides

first: Jordan

middle: S

last: Pober

first: Dan

last: Jane-wit


title: The analysis of microRNA expression in tears of Kazakh patients with climatic droplet keratopathy in Xinjiang, China

city: Shanghai

first: Zhixiang

last: Hua

address: 83 Fenyang Rd

department: Department of Ophthalmology and the Eye Institute, Eye and Ear, Nose, and Throat Hospital

institute: Fudan University

type: Non-coding RNA profiling by high throughput sequencing

summary: Climatic droplet keratopathy (CDK) is characterized by increased oil-like deposits on the anterior elastic lamina and anterior stromal layer. The pathogenic mechanisms of CDK are poorly understood. Sampling corneal tissue from CDK patients is challenging. Therefore, in this study, we analyzed the microRNA (miRNA) expression profile in tear samples of CDK patients and their putative roles in CDK pathogenesis to identify possible biomarkers.

overall_design: Basal tear fluid samples were collected from the inferior tear meniscus of both eyes using micropipettes (Shengzekanghua, China) from both the CDK and healthy control (N-CDK) groups. miRNAs extracted from tear samples of CDK and control groups were subjected to miRNA sequencing.

first: Jin

last: Yang


title: RNA seq of Wild Type, PSR1-expressing plants and PINP1-silenced plants

first: Zhan

last: Ding

address: FengLin 300

institute: CAS Center for Excellence in Molecular Plant Science

summary: Phytophthora effector PSR1 suppresses small RNA (sRNA)-mediated immunity in plants, but the underlying mechanism remains unknown. Here, we show that Phytophthora suppressor of RNA silencing 1 (PSR1) contributes to the pathogenicity of Phytophthora sojae and specifically binds to three conserved C-terminal domains of the eukaryotic PSR1-Interacting Protein 1 (PINP1). PINP1 encodes a core pre-mRNA splicing factor PRP16, which unwinds RNA duplexes and binds to pri-miRNAs and general RNAs. Intriguingly, PSR1 decreased both RNA helicase and RNA-binding activity of PINP1, thereby dampening sRNA biogenesis and RNA metabolism. The PSR1-PINP1 interaction caused global changes in alternative splicing (AS). A total of 5,135 genes simultaneously exhibited mis-splicing in both PSR1-overexpressing and PINP1-silenced plants. AS upregulated many mRNA transcripts with their introns retained. The high occurrence of intron-retention (IR) in AS-induced transcripts significantly promoted Phytophthora pathogen infection in Nicotiana benthamiana, which might be caused by the production of truncated proteins. Taken together, our findings uncover a novel role for PINP1 in regulating sRNA biogenesis and plant immunity.

overall_design: mRNA profiles of 6-week-old Wild Type, PSR1-expressing plants and PINP1-silenced plants

first: Yongli

last: Qiao


title: An inactivated multivalent influenza A virus vaccine is broadly protective in mice and ferrets [ferret]

city: Seattle

first: kathie

last: walters

state: WA

address: 401 Terry Ave N

institute: Institute for Systems Biology

summary: Influenza A viruses (IAVs) present major public health threats from annual seasonal epidemics and pandemics as well as from viruses adapted to a variety of animals including poultry, pigs, and horses. Vaccines that broadly protect against all such IAVs, so-called “universal” influenza vaccines, do not currently exist, but are urgently needed. Here, we demonstrated that an inactivated, multivalent whole virus vaccine, delivered intramuscularly or intranasally, was broadly protective against challenges with multiple IAV hemagglutinin and neuraminidase subtypes in both mice and ferrets. The vaccine is comprised of four beta-propiolactone-inactivated low pathogenicity avian influenza A virus subtypes of H1N9, H3N8, H5N1, or H7N3. Vaccinated mice and ferrets demonstrated substantial protection against a variety of IAVs, including the 1918 H1N1 strain, the highly pathogenic avian H5N8 strain, and H7N9. We also observed protection against challenge with antigenically variable and heterosubtypic avian, swine, and human viruses. Compared to mock vaccinated animals, vaccinated mice and ferrets demonstrated marked reductions in viral titers, lung pathology, and host inflammatory responses. This vaccine approach indicates the feasibility of eliciting broad, heterosubtypic IAV protection and identifies a promising candidate for influenza vaccine clinical development.

overall_design: Lung gene expression profiles from vaccinated or non-vaccinated mice and ferrets challenged with different influenza viruses were compared to lung tissue from unvaccinated, uninfected control animals.

first: Kathie-Anne

last: Walters

first: John

last: Kash

first: Jeffery

middle: K

last: Taubenberger


title: An inactivated multivalent influenza A virus vaccine is broadly protective in mice and ferrets

sample_organism:
Mustela putorius furo
Mus musculus

platform_organism:
Mustela putorius furo
Mus musculus


title: Protein phosphatase 2A propels follicular T helper cell development in lupus

city: HangZhou

first: Jiang

last: Yu

address: Yuhangtang road 866

institute: Zhejiang University

summary: To investigate the difference of gene expression in transcription level between PP2A Cα subunit knockout CD4+ T cell and WT T cell after TCR stimulation, we performed gene expression profiling analysis using data obtained from RNA-seq of the PP2A WT and CKO Naive CD4+ T cell stimulated with plate-bound CD3/CD28 for 1 hour.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for PP2A WT and KO TCR stimulated 1 hour CD4+ T cells.

first: Xu

last: Qin


title: USFs regulate the recruitment and dynamics of colocalized proteins (ChIP-Seq)

city: Bethesda

first: Yongbing

last: Zhao

state: Maryland

address: 10 Center Drive RooM 13C101A

department: NIAMS

institute: National Institutes of Health

summary: Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.

overall_design: We analyzed genome-wide binding profile of Smad3 and Smad7 in WT AND mutant mouse Ch12 cell line.

first: Andrea

last: Conte

first: Supriya

last: Vartak

first: Rafael

last: Casellas


title: Distinct sub-cellular autophagy impairments independent of protein aggregation in induced neurons from patients with Huntington disease

city: Lund

first: Johan

last: Jakobsson

address: Sölvegatan 17

department: Wallenberg Neuroscience Center

country: Sweden

institute: Lund University

summary: Huntington’s disease(HD)is a hereditary neurodegenerative disorder that is caused by CAGexpansionsin the huntingtin(HTT)gene. Modelling HD in the lab has proven challenging asrodent models poorly reproduce the disease process and cellular models fail to include age-dependent processescrucial tothe disease. Here we generatedinduced neurons(iNs)throughdirect reprogrammingof fibroblastfrombothHD-patients and healthy controls. This procedureresultedin the generation ofpatient-derived HD neurons that retainedage-dependentcharacteristics. We found that HD-iNsconsistentlydisplayedshorterandfewerneuritescomparted to ctrl-iNsandthat thisphenotypecould be rescuedbyCRISPRi-mediated silencingof mHTT.Proteomics analysis demonstrated an alteration in AMPK-signalling and autophagyin HD-iNs. In line with this,HD-iNs displayeda distinctalteration inautophagy activity,characterizedby areduction in thetransportoflate autophagic structuresfrom neurites tothecell-bodyand subsequent cargo degradation.These results identify a novel therapeutic targetfor HD and provides a rational for futuredevelopmentof CRISPR-based approaches to treatHD

overall_design:
Examination of RNA sequencing of directly reprogrammed induced neurons and adult human dermal fibroblasts from the same 7 different healthy donors and 7 different Huntington disease patients.
NOTE FROM SUBMITTER: Raw data files were not provided as they come under GDPR regulations. This is sensible data from alive individuals.

first: Karolina

last: Pircs

first: Jeovanis

last: Valdés

first: Melinda

last: Rezeli

first: Daniela

last: Grassi

first: Raquel

last: Garza

first: Yogita

last: Sharma

first: Bob

last: Hersbach

first: Kritika

first: Jessica

last: Lagerwall

first: Stina

last: Lagerström

first: Isabelle

last: St-Amour

first: Janelle

last: Drouin-Ouellet

first: Marie

last: Jönsson

first: Pia

last: Johansson

first: Kate

last: Harris

first: Romina

last: Vuono

first: Tom

last: Stoker

first: Elena

last: Cattaneo

first: Sébastien

last: Hébert

first: György

last: Marko-Varga

first: Malin

last: Parmar

first: Roger

last: Barker


title: Integrated transcriptomics and miRNAomics provide insights into the regulatory networks associated with coleoptile senescence in rice

city: New Delhi

first: Jyothish

middle: Madambikattil

last: Sasi

state: Delhi

address: BenitoJuarez Marg

department: Department of Plant Molecular Biology

country: India

institute: University of Delhi

summary:
Purpose: To understand the transcriptional changes during coleoptile senescence, transcriptome libraries were constructed from control and senescence tissues and subjected to Illumina sequencing.
Methods: Rice seeds were surface sterilized and submerged for seven days in sterile water. The seeds with coleoptile was transferred to aerobic condition. Senescence progression was monitored and tissues of un-senesced and senesced coleoptiles were harvested. Total RNA was isolated from the harvested tissues. mRNA libraries were generated and sequenced as 101 bp paired-end reads by using Illumina Hiseq 4000.
Results: Our analysis revealed that 3166 transcripts were differentially expressed in senescing coleoptile (Day 2) samples as compared to the control. Furthermore, 44 and 273 transcripts showed specific expression in control and day 2 samples, respectively. From the functional category analysis, we observed that 197, 182, 99 and 88 transcripts belonging to signalling, transcription factors, hormone signalling and transporters respectively were differentially expressed during coleoptile senescence . And 15, 12, 3, and 6 transcripts showed senescence specific expression patterns in the transporters, transcription factors, signalling and hormone signalling categories respectively.
Conclusions: The present study has generated a comprehensive resource of the molecular networks that enrich our understanding of the fundamental pathways regulating coleoptile senescence in rice.

overall_design: Transcriptome profile of coleoptile senescence in rice.

last: Madambikattil Sasi

first: Cheeni

last: VijayaKumar

first: Bharti

last: Kukreja

first: Manu

last: Agarwal

first: Surekha

last: Katiyar Agarwal


title: Single-Cell Transcriptome of Tumor-educated Lung epithelial cells

first: Yan

last: Gu

address: 800 Xiangyin Road

department: Immunology

institute: Second Miilitary Medical University

summary: We performed single-cell RNA sequencing on epithelial cells, isolated from lungs of normal and tumor-bearing mice, to shed light on the function and phenotype changes of lung epithelial cells in pre-metastatic niche.

overall_design: Lung tissues from tumor-bearing mouse and normal mouse (as a control) were digested into single-cell suspensions and CD45- SftpC+ epithelial cells were purified by FACS, followed by 10× library preparation and sequencing. All procedures were performed according to the standard manufacturer’s protocol (CG000206 RevD). Sequencing libraries were sequenced on NovaSeq6000 (Illumina) using 2x150 chemistry and quantified using a High Sensitivity DNA Chip (Agilent) on a Bioanalyzer 2100 and the Qubit High Sensitivity DNA Assay (Thermo Fisher Scientific). Single-cell RNA-seq data processing Reads were processed using the Cell Ranger 2.1.0 pipeline with default and recommended parameters.

first: Zixin

last: Wang


title: Effect of PLA2G10 treatment on activated human primary T cells.

city: West Haven

first: Tianxiang

last: Zhang

state: Connecticut

address: 600 West Campus Drive, MIC 319

summary: T lymphocytes are frequently excluded from human cancer tissue even if T cell-recruiting chemokines are present. These observations implicate the presence of T cell excluders (TCEs) in the tumor microenvironment. We report here that phospholipase A2 group 10 (PLA2G10) protein is a potent TCE to inhibit chemokine-induced T cell mobility. Overexpression of PLA2G10 is broadly found in human cancers and is associated with poor T cell infiltration in tumor tissues. Secreted PLA2G10 in the blood is correlated with the resistance to anti-programmed cell death (PD) immunotherapy in lung cancer patients. Overexpression of PLA2G10 in immunogenic mouse tumors could exclude T cells leading to their resistance to anti-PD immunotherapy. PLA2G10 hydrolyzes phospholipids into small lipid metabolites that could mediate the inhibition of T cell mobility. Our results discover a functional antagonist of chemokines, a molecular mechanism underpinning T cell exclusion in human cancer, and implicate a potential target for cancer immunotherapy.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for activated human T cells treated with CXCL11 (ITAC), PBS, PLA2G10, and CXCL11 plus PLA2G10.


title: Replacement Per and Polyfluoroalkyl Substance GenX Induces Fibroinflammatory Gene Expression in Primary Human Hepatocytes

city: Kansas City

first: Dakota

last: Robarts

state: KS

address: 3901 Rainbow Blvd

institute: University of Kansas Medical Center

summary: To goal of this study was to determine the effects of GenX on freshly isolated primary human hepatocytes (PHH).

overall_design: We exposed cultured PHH to 3 different concentrations of GenX, 0.1, 10, and 100 uM for 96 hours (n of 3 per group). Trizol was used to isolate all RNA from the PHH. RNA was then equally pooled for each group.

middle: R

first: Sumedha

last: Gunewardena

first: Udayan

last: Apte


title: Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer

first: Gary

last: Luker

address: 109 Zina Pitcher Place  A710 Biomedical Sciences Research Building

department: Radiology

summary: Patients with estrogen-receptor-positive (ER+) breast cancer, the most common subtype, remain at risk for lethal metastatic disease years after diagnosis. Recurrence arises partly because tumor cells in bone marrow become resistant to estrogen-targeted therapy. Here, we utilized a co-culture model of bone marrow mesenchymal stem cells (MSCs) and ER+ breast cancer cells to recapitulate interactions of cancer cells in bone marrow niches. ER+ breast cancer cells in direct contact with MSCs acquire cancer stem-like (CSC) phenotypes with increased resistance to standard antiestrogenic drugs. We confirmed that co-culture with MSCs increased labile iron in breast cancer cells, a phenotype associated with CSCs and disease progression. Clinically approved iron chelators and in-house lysosomal iron-targeting compounds restored sensitivity to antiestrogenic therapy. These findings establish iron modulation as a mechanism to reverse MSC-induced drug resistance and suggest iron modulation in combination with estrogen-targeted therapy as a promising, translatable strategy to treat ER+ breast cancer.

overall_design: Co-culture model of bone marrow mesenchymal stem cells (MSCs) and ER+ breast cancer cells. Co-cultured cancer and stromal cells were separated before performing RNA sequencing. Data sets also include monoculture samples of cancer and stromal cells as well as cancer cells with conditioned medium from stromal cells.

first: Johanna

middle: M

last: Buschhaus

first: Shrila

last: Rajendran

first: Brock

last: Humphries

first: Alyssa

last: Cutter

first: Ayşe

last: Muñiz

first: Nicholas

last: Ciavattone

first: Alexander

first: Tatiana

last: Cañeque

first: Zeribe

last: Nwosu

first: Debashis

last: Sahoo

first: Avinash

last: Bevoor

first: Yatrik

last: Shah

first: Costas

last: Lyssiotis

first: Pradipta

last: Ghosh

first: Max

last: Wicha

first: Raphaël

last: Rodriguez


title: Chromatin binding of AR/TEAD/H3K27ac in C4-2 Cells

city: Dallas

first: Xu

last: Li

state: Texas

address: 6000 Harry Hines Blvd.

department: Molecular Biology

institute: University of Texas Southwestern Medical Center at Dallas

summary: We report TEAD could facilitate AR binding to its target loci

overall_design: Examination of AR, TEAD and H3K27ac chromatine binding signal in C4-2 cells.


title: Next Generation Sequencing Facilitates Quantitative Analysis of SKOV3 cells overexpression of TNFAIP8L2

city: Jinan

first: Shuai

last: Xu

state: Shandong

address: 247 North Park Street

department: Obstetrics and Gynecology

institute: Second hospital of Shandong University

summary: Purpose: Next generation sequencing (NGS) has revolutionized system-based analysis of cellular pathways. The goals of this study are to compare NGS-derived transcriptome profiling of human ovarian cancer cell, SKOV3 cells after endogenous overexpression of TNFAIP8L2 (TIPE2) . Methods: We constructed TIPE2 overexpression SKOV3 cell lines and control vector cell lines with lentivirus. Then the NGS based deep sequencing analysis was generated in triplicate to analyze the critical downstream targets after TIPE2 overexpression using ILLumina GAIIx. Results: The differentially expressed genes were identified using an optimized data analysis workflow, and we identified 49 upregulated and 28 downregulated genes in the SKOV3/TIPE2 group compared with the vector group using a  |log2Foldchange|﹥0 and p < 0.05. Conclusions: Our study represents the first detailed analysis of transcriptomes in ovarian cancer cell line after overexpression of TIPE2 by RNA-seq technology.

overall_design: mRNA profiles of SKOV3 cell overexpression of TIPE2

first: Xiaolin

last: Gao

first: Shiqian

last: Zhang

first: Fanzhen

last: Hong


title: Next Generation Sequencing Facilitates Quantitative Analysis of Ern1f/f and Ern1f/f AKO iWAT transcriptomes

city: wuhan

first: Yong

last: Liu

address: Bayi road

department: College of Life Sciences

institute: Wuhan university

summary: Bulk RNA-seq has uncovered the the function of adipocyte IRE1α in cold-induced thermogenic program in inguinal white adipose tissue. The GO analysis shows that adipocyte IRE1α supressed inflammatory responds when the mice were maintained at 30oC and adipocyte IRE1α abrogation facilated cold-induced thermogenic program after challenged with cold stress. In addition, the transcription factor (TF) analysis indicates that adipocyte IRE1α repressed lots of temperature-dependent TFs, including PGC1α.

overall_design: There are 4 groups (AKO30C, AKO8C, WT30C, WT8C) and 3 mice each group.

last: Chen


title: Functionality of stripe factors on chromatin accessibility (ChIP-Seq)

first: Yongbing

last: Zhao

overall_design: We have knocked out stripe factors individually or combinatorically in ch12 cell line and then checked their functionality on chromatin accessibility.

first: Andrea

last: Conte

first: Supriya

last: Vartak

first: Rafael

last: Casellas


title: MicroRNA expression profile from retinoblastoma tumors and pediatric controls

city: Bangalore

first: Vishnu

last: Suresh Babu

state: Karnataka

address: NH Health city, Bommasandra

department: Narayana Nethralaya Foundation

institute: GROW Research Laboratory

summary: To discover differentially expressed microRNA's in Rb tumors compared to pediatric retina

overall_design: Nine enucleated human retinoblastoma tumors and two pediatric retina controls used for the study. Total RNA was isolated from 9 Rb tumors and 2 control pediatric retina samples using Agilent Absolutely RNA miRNA kit. Twenty-five nanograms of RNA from Rb tumors and control pediatric retina samples were labeled with Cy3 dye using an Agilent Low Input Quick Amp Labeling Kit

first: Arkasubhra

first: Nilanjan

last: Guha


title: Effect of mithramycin on chromatin accessibility (ChIP-Seq)

overall_design: We displaced stripe factors with mithramycin in activated B cell and then checked effect on chromatin accessibility.


title: An inactivated multivalent influenza A virus vaccine is broadly protective in mice and ferrets [mouse]

first: kathie

last: walters

first: Kathie-Anne

last: Walters

first: John

last: Kash

first: Jeffery

last: Taubenberger


title: SNP effect on chromatin accessibility (ChIP-Seq)

overall_design: We check SNP effect on chromatin accessibility in different mouse F1 cells.


title: Integrated analysis of transcriptome and histone modifications in granulosa cells during ovulation in female mice [ChIP-seq]

city: Ube

first: Yuichiro

last: Shirafuta

state: Yamaguchi

address: 1-1-1, minami-kogushi

country: Japan

institute: Yamaguchi university

summary: The ovulatory LH surge induces rapid changes of transcriptome and cellular functions in granulosa cells (GCs) undergoing luteinization.  However, it remains unclear how the changes in genome-wide gene expression are regulated.  The changes of trimethylation of lysine 4 on histone H3 (H3K4me3) is associated with the rapid alteration of gene expression.  In this study, we genome-widely investigated the changes of transcriptome and H3K4me3 status in mouse GCs undergoing luteinization during ovulation.  GCs were obtained from mice treated with equine chorionic gonadotropin (eCG) before, 4 h and 12 h after human (h)CG injection.  RNA-sequence identified a number of up- or down-regulated genes, which can be classified into six patterns according to the time-course changes of gene expression.  A number of genes showed a transient up- or down-regulation at 4 h after hCG stimulation.  Gene ontology analysis revealed that they were involved in the regulation of steroidogenesis, ovulation, COC expansion, angiogenesis, immune system, ROS metabolism, inflammatory response, and metabolisms.  The newly identified cellular functions, DNA repair, autophagy and cell growth were found to be activated during ovulation.  ChIP-sequence revealed a genome-wide and rapid change of H3K4me3 during ovulation.  Integration of transcriptome and H3K4me3 data identified a number of H3K4me3-regulated genes, which were involved in the regulation of a lot of cellular functions for ovulation and luteinization.  The present study demonstrated that genome-wide changes of H3K4me3 might contribute to the rapid change of genome-wide gene expression, which enables GCs acquire a lot of cellular functions within a short time for ovulation and luteinization.

overall_design: ChIP-seq profiles of mouse granulosa cells undergoing luteinization during ovulation

first: Isao

last: Tamura

first: Norihiro

last: Sugino


title: Targeting human langerin promotes HIV-1 specific humoral immune responses

city: Créteil

first: cecile

last: lefebvre

address: 51 Avenue du Marechal De Lattre de Tassigny

country: France

institute: INSERM U955_VRI

summary: The main avenue for the development of an HIV-1 vaccine remains the induction of protective antibodies. A rationale approach is to target antigen to specific receptors on dendritic cells (DC) via fused monoclonal antibodies (mAb). In mouse and non-human primate models, targeting of skin Langerhans cells (LC) with anti-Langerin mAbs fused with HIV-1 Gag antigen drives antigen-specific humoral responses. The development of these immunization strategies in humans requires a better understanding of early immune events driven by human LC. We therefore produced anti-Langerin mAbs fused with the HIV-1 gp140z Envelope (αLC.Env). First, we show that primary skin human LC and in vitro differentiated LC induce differentiation and expansion of naïve CD4+ T cells into T follicular helper (Tfh) cells. Second, when human LC are pre-treated with αLC.Env, differentiated Tfh cells significantly promote the production of specific IgG by B cells. Strikingly, HIV-Env-specific Ig are secreted by HIV-specific memory B cells. Consistently, we found that receptors and cytokines involved in Tfh differentiation and B cell functions are upregulated by LC during their maturation and after targeting Langerin. Finally, we show that subcutaneous immunisation of mice by αLC.Env induces germinal center (GC) reaction in draining lymph nodes with higher numbers of Tfh cells, Env-specific B cells, as well as specific IgG serum levels compared to mice immunised with the non-targeting Env antigen. Altogether, we provide evidence that human LC properly targeted may be licensed to efficiently induce Tfh cell and B cell responses in GC.

overall_design: RNAseq analysis on primary skin LC. Epidermal LC of 6 healthy donors were isolated either at steady state or after 3 days of migration in culture.

first: Jérôme

last: KERVEVAN

first: Cécile

last: LEFEBVRE

first: Hakim

last: Hocini

first: Sylvain

last: CARDINAUD

first: Yves

last: LEVY


title: hnRNP R negatively regulates transcription by modulating the association of P-TEFb with 7SK and BRD4

city: Würzburg

first: Tom

last: Gräfenhan

address: Josef-Schneider-Str. 2, Bau D15

department: Core Unit SysMed

institute: University of Wuerzburg

summary: The P-TEFb complex promotes transcription elongation by releasing paused RNA polymerase II. P-TEFb itself is known to be inactivated through binding to the non-coding RNA 7SK but there is only limited information about mechanisms regulating their association. Here, we show that cells deficient in the RNA-binding protein hnRNP R, a known 7SK interactor, exhibit increased transcription due to phosphorylation of RNA polymerase II. Intriguingly, loss of hnRNP R promotes the release of P-TEFb from 7SK, accompanied by enhanced hnRNP A1 binding to 7SK. Additionally, we found that hnRNP R interacts with BRD4, and that hnRNP R depletion increases BRD4 binding to the P-TEFb component CDK9. Finally, CDK9 is stabilized upon loss of hnRNP R and its association with Cyclin K is enhanced. Together, our results indicate that hnRNP R negatively regulates transcription by modulating the activity and stability of the P-TEFb complex, exemplifying the multimodal regulation of P-TEFb by an RNA-binding protein.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for HNRNPR+/+ and -/-, and for 7SK+/+ and -/- cells.

first: Changhe

last: Ji

first: Chunchu

last: Deng

first: Katharina

last: Antor

first: Thorsten

last: Bischler

first: Cornelius

last: Schneider

first: Utz

last: Fischer

first: Michael

last: Sendtner

last: Briese


title: Integrated transcriptomics and miRNAomics provide insights into the regulatory networks associated with coleoptile senescence in rice.

first: Jyothish

last: Sasi

summary:
Purpose: To understand the miRNAome changes during coleoptile senescence, small RNA libraries were constructed from control and senescence tissues and subjected to Illumina sequencing.
Methods: Rice seeds were surface sterilized and submerged for seven days in sterile water. The seeds with coleoptile was transferred to aerobic condition. Senescence progression was monitored and tissues of un-senesced and senesced coleoptiles were harvested. Total RNA was isolated from the harvested tissues. Total four small RNA libraries of coleoptile senescence were constructed and high-throughput sequencing was performed using Illumina GA IIx system .  .
Results: Small RNA sequencing identified forty-one known and twenty-one novel miRNAs that were differentially expressed during coleoptile senescence. Integration of expression data of transcriptome and miRNAome identified 148 miRNA-mRNA modules, mainly comprised of miRNAs regulating TFs, signaling-associated factors and transporters, thereby demonstrating multi-tiered regulation of coleoptile senescence.
Conclusions: The present study has generated a comprehensive resource of the molecular networks that enrich our understanding of the fundamental pathways regulating coleoptile senescence in rice.

overall_design: miRNAomic profile of coleoptile senescence in rice.

last: Madambikattil Sasi

first: Cheeni

last: VijayaKumar

first: Bharti

last: Kukreja

first: Manu

last: Agarwal

first: Surekha

last: Katiyar Agarwal


title: SNP effect on chromatin accessibility (RNA-Seq)

first: Yongbing

last: Zhao

first: Andrea

last: Conte

first: Supriya

last: Vartak

first: Rafael

last: Casellas


title: SNP effect on chromatin accessibility (ATAC-Seq)


title: Transcriptome Sequencing of Tumor-educated Lung Epithelial Cells in the Pre-metastatic Niche

first: Yan

last: Gu

summary: We performed transcriptome sequencing on epithelial cells, isolated from lungs of normal and tumor-bearing mice, to shed light on the function and phenotype changes of lung epithelial cells in the pre-metastatic niche.

overall_design: Lung tissues from tumor-bearing mouse and normal mouse (as a control) were digested into single-cell suspensions and CD45- SftpC+ epithelial cells were purified by FACS, followed by transcriptome sequencing. All procedures were performed according to the standard manufacturer’s protocol. The total RNA samples are first treated with DNase I to degrade any possible DNA contamination. Then the mRNA is enriched by using the oligo(dT) magnetic beads (for eukaryotes). Mixed with the fragmentation buffer, the mRNA is fragmented into short fragments (about 200 bp). Then the first strand of cDNA is synthesized by using random hexamer-primer. Buffer, dNTPs, RNase H and DNA polymerase I are added to synthesize the second strand. The double strand cDNA is purified with magnetic beads. End reparation and 3'-end single nucleotide A (adenine) addition is then performed. Finally, sequencing adaptors are ligated to the fragments. The fragments are enriched by PCR amplification. During the QC step, Agilent 2100 Bioanaylzer and ABI StepOnePlus Real-Time PCR System are used to qualify and quantify of the sample library. The library products are ready for sequencing via Illumina HiSeqTM 2000 or other sequencer when necessary.

first: Zixin

last: Wang


title: TF ChIP-seq from GM12878 (ENCSR057DTZ)

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
GM12878 immortalized cell line stably expressing C-terminal eGFP-ZBTB11 fusion protein.

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: Effect of mithramycin on chromatin accessibility (RNA-Seq)

summary: Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.


title: SNP effect on chromatin accessibility (Whole genome sequencing)

type: Genome variation profiling by high throughput sequencing


title: Functionality of stripe factors on chromatin accessibility (ATAC-Seq)


title: Functionality of stripe factors on chromatin accessibility (RNA-Seq)


title: Comprehensive maps of transcription factor (TF) binding sites in mouse (RNA-Seq)

overall_design: Integrated analysis of chromatin accessibility and transcriptome data from mouse primary cells and tissues.


title: β cell specific Crif1 haploinsufficiency effect.

city: Jung-gu

first: hyunjung

last: hong

state: Daejeon

address: Munhwaro 222

department: biomedical

country: South Korea

institute: Chungnam national university

summary: CRIF1 is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane. Beta cell specific Crif1 haploinsufficiency resulted in defect of first phase insulin secretion, and caused islet cell composition change as well as proliferation of beta cell for a compensation to maintain metabolic homeostasis. These results suggest that mitochondrial OxPhos function of beta cell has roles for beta cell compensation as well as insulin secretion.

overall_design: Islet mRNA profiles of 14 weeks old Control and Crif1beta+/-

first: Hyunjung

last: Hong

first: Hyunjin

last: Kim

first: Minho

last: Shong


title: The ELK3-CXCL16 axis regulates NK cell cytotoxicity via the chemotactic activity of CXCL16 in TNBC

status: Public on Jul 20 2022

city: Seongnam-si

first: Dae-keum

last: Lee

state: Gyeonggi-do

address: 335, Pangyo-ro,  Bundang-gu

institute: CHA university

summary:
Background Triple-negative breast cancer (TNBC) is the most challenging subtype of breast cancer because of its aggressive behavior and the limited therapeutic strategies available. In the last decade, immunotherapy has become a promising treatment to prolong survival in advanced solid cancers including TNBC. However, the efficacy of immunotherapy in solid cancers remains limited because solid tumors contain few tumor-infiltrating lymphocytes.
Methods A proteome profiler array was performed to identify secreted CXCL16 protein, the expression of which is regulated by ELK3 to control natural killer (NK) cell-mediated cytotoxicity.  The correlation between ELK3 and CXCL16 was investigated by microarray and TCGA data analysis. NK cell cytotoxicity and migration assays were performed to examine the role of ELK3-CXCL16 in regulating the anticancer effect in TNBC. CXCL16-mediated NK cell recruitment and NK cell cytotoxicity were examined in an experimental metastasis mouse model and in an MDA-MB231 orthotopic mouse model.
Results We show that targeting the ETS transcription factor ELK3 recruits immune cells including NK cells into tumors via the chemotactic activity of the chemokine.  ELK3 depletion upregulated CXCL16 expression, thereby inducing NK cell recruitment to tumors and increasing NK cell cytotoxicity in TNBC . In silico analysis showed that ELK3 is negatively correlated with CXCL16 expression in breast cancer patient samples. Low expression of ELK3 and high expression of CXCL16 were associated with a better prognosis. Low expression of ELK3 and high expression of CXCL16 were associated with increased expression of NK cell-related genes.
Conclusions The ELK3-CXCL16 axis regulates NK cell recruitment and increases NK cell cytotoxicity, suggesting that targeting the ELK3 gene could be an adjuvant strategy for increasing the efficacy of immunotherapy in TNBC.

overall_design: Affymetrix expression microarray analysis of the Hs578T cell line was performed by BioCore. Briefly, a library  was constructed using the standard Affymetrix protocol. Labeled DNA was hybridized to the Affymetrix GeneChip Array (Affymetrix, Santa Clara, CA, USA) and scanned on a GCS3000 scanner (Affymetrix). Data processing and analysis were performed using Affymetrix GeneChip Command Console Software (Affymetrix). Genes with fold change >1.50 and p <0.05 were first selected. Gene lists were sorted using the KEGG mapper tool (https://www.genome.jp/kegg/mapper/). Gene clustering and heatmaps were analyzed using the MeV tool (version 4.9.0). The Hs578T microarray data are deposited in the Gene Expression Omnibus data repository under the code GSEXXXXX. Gene expression data from breast cancer cell lines were downloaded from Cancer Dependency Map (DepMap). Gene expression data were obtained from 24 breast cancer cell lines.

first: Hae-Yun

last: Jung

first: Dae-Keum

first: Minwook

first: Seung

middle: H

last: Choi

first: Joo

last: Park

first: Eun-Su

last: Ko

first: Jongwon

first: Kyung-Soon


title: Integrated analysis of transcriptome and histone modifications in granulosa cells during ovulation in female mice

first: Yuichiro

last: Shirafuta

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

overall_design: Refer to individual Series


title: Integrated analysis of transcriptome and histone modifications in granulosa cells during ovulation in female mice [RNA-seq]

overall_design: mRNA profiles of mouse granulosa cells undergoing luteinization during ovulation

first: Isao

last: Tamura

first: Norihiro

last: Sugino


title: Molecular Epidemiology of Enterobacterales Resistant to Antibiotics of Last Resort in Pregnant Women in Labour at a Tertiary Hospital

city: Pretoria

first: John

last: Osei Sekyere

state: Gauteng

address: 05 Bopheloweg Off Dr. Savage Road

department: Department of Medical Microbiology

country: South Africa

institute: University of Pretoria

type: Methylation profiling by high throughput sequencing

summary: This study aims to determine the epidemiology of Enterobacteriaceae resistant to antibiotics of last resort in pregnant women in labour at a tertiary hospital, Pretoria, South Africa. Rectal swabs shall be used to screen for colonisation with CRE and colistin-resistant Enterobacteriales in pregnant women during labour.    Carbapenem and colistin-resistant Enterobacterales can cause the following infections: bacteraemia; nosocomial pneumonia; urinary tract infections, and intra-abdominal infections. Due to limited treatment options, infections caused by these multidrug-resistant organisms are associated with a mortality rate of 40-50%. Screening for colonisation of carbapenem-resistant Enterobacteriaceae (CRE) and colistin-resistant Enterobacteriaceae will help implement infection and prevention measures to limit the spread of these multidrug-resistant organisms.

sample_organism:
Enterobacter cloacae
Klebsiella pneumoniae
Enterobacter roggenkampii

overall_design: Genomic and epigenomic characterisation of carbapenem- and colistin-resistant Enterobacter spp. & K. pneumoniae

first: Virginia

last: Ntsoane

first: Nontombi

last: Mbelle

middle: O

last: Sekyere


title: Effect of uterine-derived extracellular vesicles on trophoblast cells

city: Olsztyn

first: Monika

last: Kaczmarek

address: Tuwima 10

country: Poland

institute: Institute of Animal Reproduction and Food Research, Polish Academy of Sciences

summary: Recently, extracellular vesicles, nanoparticles able to transfer functionally active cargo between cells, have emerged as important players in cell–cell communication, and as such, they have gained great attention over the past decade also in reproductive biology. To get a broader picture of transcriptomic changes evoked by extracellular vesicles cells in porcine conceptuses, trophoblast primary cells were exposed in vitro to uterine-derived extracellular vesicles (EVs).

overall_design: Porcine trophoblast primary cells were treated in vitro with the uterine-derived EVs collected from the same female on day 16 of pregnancy. Then, comparative gene expression profiling analysis of RNA-seq data for porcine primary trophoblast cells was performed.

first: Joanna

last: Szuszkiewicz

first: Kamil

last: Myszczynski


title: Effect of Swimming on gene expression of AOM/DSS induced colitis associated cancer mice

city: shanghai

first: weiyi

last: wang

address: No. 1111 Xianxia Road, Changning District, Shanghai, PR China

department: Department of Endoscopy

institute: Shanghai Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

summary: To investigate the inhibitory function of Swimming in the tumor formation in CAC mice, we established  AOM/DSS induced CAC mice in which mice were pretreated with swimming exercise.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for Colorectal tissue of CAC mice, its Swimmimg pretreatment group, ctrl group and ctrl_ swim group. We then detected the enriched KEGG pathway analysis using data obtained from RNA-seq of SH-SY5Y.

first: Weiyi

last: Wang


title: Altered regulation of mRNA and miRNA expression in epithelial and stromal tissue of keratoconus corneas [miRNA]

city: Homburg

first: Tanja

last: Stachon

address: Kirrergerstr. 100

department: Dr. Rolf  M. Schwiete Center

institute: Saarland University

summary: Purpose:  To evaluate conjunctival cell microRNA and mRNA expression in relation to observed phenotype and genotype of aniridia-associated keratopathy (AAK) in a cohort of subjects with congenital aniridia.  Methods:  Using impression cytology, bulbar conjunctival cells were sampled from 20 subjects with congenital aniridia and 20 age and sex-matched healthy control subjects. RNA was extracted and microRNA and mRNA analysis was performed using microarrays. Results were related to the presence and severity of AAK determined by a standardized clinical grading scale and to the genotype (PAX6 mutation?) determined by clinical genetics.   Results:  Of the 2549 microRNAs analyzed, 21 were differentially expressed relative to controls. Among these miR-204-5p, an inhibitor of corneal neovascularization, was downregulated 26.8-fold, while miR-5787 and miR-224-5p were upregulated 2.8 and 2.4-fold relative to controls, respectively. At the mRNA level, 539 transcripts were differentially expressed, among these FOSB and FOS were upregulated 17.5 and 9.7-fold respectively, and JUN by 2.9-fold, all components of the AP-1 transcription factor complex. Pathway analysis revealed dysregulation of several enriched pathways including PI3K-Akt, MAPK, and Ras signaling pathways in aniridia. For several microRNAs and transcripts, expression levels aligned with AAK severity, while in very mild cases with missense or non-PAX6 coding mutations, gene expression was only minimally altered.  Conclusion:  In aniridia, specific factors and pathways are strongly dysregulated in conjunctival cells, suggesting that the conjunctiva in aniridia is abnormally maintained in a pro-angiogenic and proliferative state, promoting the aggressivity of AAK in a mutation-dependent manner. Transcriptional profiling of conjunctival cells at the microRNA and mRNA levels presents a powerful, minimally-invasive means to assess the regulation of cell dysfunction at the ocular surface.

overall_design: MiRNA and mRNA expression profiles of epithelial and stromal cells from 8 patients with keratoconus compared to controls

first: Nicole

last: Ludwig


title: Altered regulation of mRNA and miRNA expression in epithelial and stromal tissue of keratoconus corneas

type:
Non-coding RNA profiling by array
Expression profiling by array


title: Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

city: Brussels

first: Viridiane

last: Gratpain

address: avenue Emmanuel Mounier 73

department: Louvain Drug Research Institute

country: Belgium

institute: Université Catholique de Louvain

summary: To investigate the impact of a pro-inflammatory stimulus (TNFα and IFNγ, 20 ng/ml) on miRNA in SCAP-EV, we isolated EV from non-activated and activated SCAP  and then extracted miRNA

overall_design: Comparative miRNA expression between EV from non-activated SCAP and EV from activated SCAP (activation with TNFα and IFNγ). We replicated this experiment 3 times.

first: Anne

last: des Rieux

first: Axelle

last: Loriot

first: Pauline

last: Bottemane

first: Ludovic

last: d'Auria

first: Romano

last: Terrasi

first: Valery

last: Payen

first: Vincent

last: van Pesch

first: Giulio

last: Muccioli


title: Effect of mithramycin on chromatin accessibility (ATAC-Seq)

city: Bethesda

first: Yongbing

last: Zhao

address: 10 Center Drive RooM 13C101A

institute: National Institutes of Health

overall_design: We displaced stripe factors with mithramycin in activated B cell and then checked effect on chromatin accessibility.

first: Andrea

last: Conte

first: Supriya

last: Vartak

first: Rafael

last: Casellas


title: Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice

city: New York City

first: Florencia

last: Schlamp

state: New York

address: 435 East 30th Street

institute: NYU Langone Health

summary: The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression.

overall_design: CD68+ cells were selected from atherosclerotic plaques from WT and Prmt2-/- mice undergoing regression by laser capture microdissection (LCM). Foam cells were identified under a microscope and verified by positive CD68 staining. For each animal, CD68+ cells were captured from 50–60 frozen sections. RNA was isolated and RNA -seq was performed to determine genes differentially expressed in WT and Prmt2-/-  CD68+ cells under non-diabetic conditions.

first: Beyza

last: Vurusaner

first: Prashanth

last: Thevkar-Nages

first: Ravneet

last: Kaur

first: Chiara

last: Giannarelli

first: Michael

last: Garabedian

first: Edward

last: Fisher


title: Regulation of metablism by mitochondrial MUL1 E3 ubiquitin ligase

city: Orlando

first: Antonis

last: Zervos

state: FL

address: 12722 Research Pkwy

department: Burnett School of Biomedical Sciences

institute: University of Central Florida

summary: To investigate how the absence of MUL1 affects metabolic changes as reflected by gene expression.

overall_design:
We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells in triplicates.
Comparative gene expression profiling analysis of RNA-seq data for HEK293 cells and its KO derivatives (MUL1-/-).

first: Lucia

last: Cilenti


title: PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [RNA-Seq]

city: Los Angeles

first: Hideki

last: Furuya

address: 110 N. George Burns Road, Davis 2025

department: Surgery

institute: Cedars Sinai Medical Center

summary: The extracellular activity of Plasminogen activator inhibitor-1 (PAI-1) is well described, acting as an inhibitor of tissue plasminogen activator and urokinase-type plasminogen activator, impacting fibrinolysis. Recent studies have revealed a pro-tumorigenic role of PAI-1 in human cancers, via the regulation of angiogenesis and tumor cell survival. In this study, immunohistochemical staining of 939 human bladder cancer specimens showed that PAI-1 expression levels correlated with tumor grade, tumor stage and overall survival. The typical subcellular localization of PAI-1 is cytoplasmic, but in approximately a quarter of the cases, PAI-1 was observed to be localized to both the tumor cell cytoplasm and the nucleus. To investigate the potential function of nuclear PAI-1 in tumor biology we applied chromatin immunoprecipitation (ChIP)-sequencing, gene expression profiling, and rapid immunoprecipitation mass spectrometry to a pair of bladder cancer cell lines. ChIP-sequencing revealed that PAI-1 can bind DNA at distal intergenic regions, suggesting a role as a transcriptional coregulator. The downregulation of PAI-1 in bladder cancer cell lines caused the upregulation of numerous genes, and the integration of ChIP-sequence and RNA-sequence data identified 57 candidate genes subject to PAI-1 regulation. Taken together, the data suggest that nuclear PAI-1 can influence gene expression programs and support malignancy.

overall_design: We trnasfected scrambled or PAI-1 siRNA in 2 human bladder cancer cell lines, and then performed RNA-seq

first: Charles

last: Rosser


title: PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity


title: Small RNA profiles of mouse leptotene/zygotene spermatocytes at postnatal day 11 and 16.

city: Nagoya

first: Kenji

last: Ichiyanagi

address: Furo-cho, Chikusa-ku

department: Graduate School of Bioagricultural Sciences

institute: Nagoya University

summary: Leptotene and zygote (LZ) spematocytes at P11, P16, and P21 were compared by small-RNA-seq. The P21 data has been published under GSE70891. This revealed that, the late piRNA clusters were rarely expressed in P11 LZ spermatocytes, but  started to be expressed at P16. Whereas previous reports analysing testicular RNAs showed that "prepachytene" piRNAs are short (25–28 nt) , this study revealed that piRNAs derived from the late piRNA clusters in P16 and P21 LZ spermatocytes contained both short (25–28 nt) and long (29–31 nt) piRNAs.

overall_design: Leptotene and zygote spematocytes were  purified by cell sorting using Hochyst staining from testes of male mouse (C57BL/6J) at postnataldays 11 and 16.  RNA were extracted by isogene, and used for small RNA  library preparation. The libraries were sequenced by MiSeq.

first: Masaki

last: Kawase


title: Epigenetic activation of antiviral sensors and effectors of interferon response pathways during SARS-CoV-2 infection

city: Szczecin

first: Tomasz

last: Wojdacz

state: Zachodniopomorskie

address: Unii Lubelskiej 1

department: Independent Clinical Epigenetics Laboratory

institute: Pomeranian Medical University

type: Methylation profiling by genome tiling array

summary: We combined methylomics and transcriptomics data from four geographically distant and ethnically heterogeneous cohorts of COVID-19 patients, with the aim to assess causal interaction of SARS-CoV-2 virus with host methylome.

overall_design: Bisulfite converted DNA isolated from peripheral blood from 32 COVID-19 patients were run on the Infinium MethylationEPIC platform.

first: Jan

last: Bińkowski

first: Olga

last: Taryma-Leśniak

first: Karolina

last: Łuczkowska

first: Anna

last: Niedźwiedź

first: Kacper

last: Lechowicz

first: Katarzyna

last: Kotfis

first: Bogusław

last: Machaliński

first: Miłosz

last: Parczewski