title: DNase-seq from cerebellum (ENCSR176CFX)


title: ATAC-seq from spleen (ENCSR182VGJ)

status: Public on Oct 16 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:
ATAC-seq on human spleen

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: ATAC-seq from bile duct (ENCSR174MLD)

summary:
ATAC-seq on human bile duct

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: ATAC-seq from spleen (ENCSR979TCG)


title: DNase-seq from HCT116 (ENCSR521WNU)

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: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR304CXS)


title: ATAC-seq from kidney (ENCSR297VGU)

summary:
ATAC-seq on human kidney

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: DNase-seq from HCT116 (ENCSR163KCQ)


title: ATAC-seq from cardiac septum (ENCSR167SYF)

summary:
ATAC-seq on human cardiac septum

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: ATAC-seq from central memory CD8-positive, alpha-beta T cell (ENCSR165FYY)


title: DNase-seq from kidney (ENCSR170FAP)


title: ATAC-seq from spleen (ENCSR158KCS)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR302MYX)


title: DNase-seq from lung (ENCSR293SQC)


title: ATAC-seq from aorta (ENCSR295TFY)

summary:
ATAC-seq on human aorta

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: DNase-seq from layer of hippocampus (ENCSR154CWQ)


title: ATAC-seq from psoas muscle (ENCSR154UWN)

summary:
ATAC-seq on human psoas muscle

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: DNase-seq from CD8-positive, alpha-beta memory T cell (ENCSR295UXT)


title: DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR291HMM)


title: DNase-seq from lung (ENCSR285LPX)


title: DNase-seq from right cerebral cortex (ENCSR293BBH)


title: WGBS from motor neuron (ENCSR149NZN)

type: Methylation profiling by high throughput sequencing

summary:
Whole genome bisulfite-seq on human motor neuron cell lines derived from neural progenitor cells: Control CS14 - iNPC

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: DNase-seq from HCT116 (ENCSR702VYW)


title: ATAC-seq from uterus (ENCSR705RZX)

summary:
ATAC-seq on human uterus

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: DNase-seq from HCT116 (ENCSR694YJR)


title: DNase-seq from left cerebral cortex (ENCSR282IXW)


title: DNase-seq from frontal cortex (ENCSR280ZEI)


title: DNase-seq from immature natural killer cell (ENCSR696ZDW)


title: DNase-seq from lung (ENCSR702AVR)


title: DNase-seq from layer of hippocampus (ENCSR270DJQ)


title: DNase-seq from activated naive CD8-positive, alpha-beta T cell (ENCSR518YYX)


title: ATAC-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR513EVP)


title: DNase-seq from activated naive CD4-positive, alpha-beta T cell (ENCSR515PDV)


title: ATAC-seq from spleen (ENCSR694OWY)


title: ATAC-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR260LAN)


title: DNase-seq from Caco-2 (ENCSR255STJ)


title: DNase-seq from left cerebral cortex (ENCSR255QUX)


title: DNase-seq from urinary bladder (ENCSR690LVC)


title: DNase-seq from right cerebral cortex (ENCSR690IQA)


title: ATAC-seq from T-helper 17 cell (ENCSR248ZAC)


title: DNase-seq from layer of hippocampus (ENCSR254KUF)


title: DNase-seq from frontal cortex (ENCSR687OIL)


title: DNase-seq from HCT116 (ENCSR975SCL)


title: DNase-seq from HCT116 (ENCSR690ADK)


title: DNase-seq from spleen (ENCSR146PAW)


title: DNase-seq from heart (ENCSR147AIN)


title: DNase-seq from layer of hippocampus (ENCSR247PTA)


title: ATAC-seq from upper lobe of left lung (ENCSR242QRV)

summary:
ATAC-seq on human upper lobe of left lung

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: DNase-seq from CD4-positive, alpha-beta memory T cell (ENCSR977UMU)


title: DNase-seq from natural killer cell (ENCSR975LGK)


title: DNase-seq from spleen (ENCSR145GGC)


title: DNase-seq from thymus (ENCSR133BTF)


title: WGBS from motor neuron (ENCSR675UVC)

summary:
Whole genome bisulfite-seq on human motor neuron cell lines derived from neural progenitor cells: Control SMA - iNPC

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: DNase-seq from chondrocyte (ENCSR970DQR)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR969QKG)


title: ATAC-seq from K562 (ENCSR956DNB)

summary:
ATAC-seq on K562 cells stained for GATA1 and sorted for highest 15% of expression

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: DNase-seq from HCT116 (ENCSR129EWE)


title: DNase-seq from central memory CD4-positive, alpha-beta T cell (ENCSR234FTX)


title: DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR953OBW)


title: DNase-seq from right cerebral cortex (ENCSR952RWH)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR232NLA)


title: DNase-seq from layer of hippocampus (ENCSR235KWU)


title: ATAC-seq from liver (ENCSR124NNL)

summary:
ATAC-seq on human liver

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: DNase-seq from memory B cell (ENCSR229BGG)


title: DNase-seq from ovary (ENCSR232ELD)


title: ATAC-seq from left cardiac atrium (ENCSR736CIN)

summary:
ATAC-seq on human left cardiac atrium

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: DNase-seq from T-helper 2 cell (ENCSR223XND)


title: ATAC-seq from heart left ventricle (ENCSR225FZH)

summary:
ATAC-seq on human heart left ventricle

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: DNase-seq from right cerebral cortex (ENCSR224FBA)


title: DNase-seq from endodermal cell (ENCSR940CXU)


title: DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR938OKL)


title: DNase-seq from cerebellum (ENCSR934ECT)


title: DNase-seq from heart (ENCSR944NVO)


title: DNase-seq from A673 (ENCSR114QAK)


title: ATAC-seq from left ventricle myocardium inferior (ENCSR946MAI)

summary:
ATAC-seq on human left ventricle myocardium inferior

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: DNase-seq from gastrocnemius (ENCSR976MHB)


title: DNase-seq from gastrocnemius (ENCSR115SWG)


title: DNase-seq from cerebellum (ENCSR502NYH)


title: WGBS from motor neuron (ENCSR222DHK)

summary:
Whole genome bisulfite-seq on human motor neuron cell lines derived from neural progenitor cells: ALS-52 - iPSC

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: DNase-seq from gastrocnemius (ENCSR498SCU)


title: DNase-seq from H1 (ENCSR951BNY)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR125OEJ)


title: DNase-seq from activated B cell (ENCSR109DTU)


title: ATAC-seq from lower lobe of right lung (ENCSR923VTG)

summary:
ATAC-seq on human lower lobe of right lung

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: DNase-seq from left cerebral cortex (ENCSR106PXP)


title: DNase-seq from urinary bladder (ENCSR105BDM)


title: ATAC-seq from heart right ventricle (ENCSR491VKV)

summary:
ATAC-seq on human heart right ventricle

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: DNase-seq from stimulated activated effector memory CD8-positive, alpha-beta T cell (ENCSR917BSW)

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: DNase-seq from heart (ENCSR104ZBW)


title: DNase-seq from excitatory neuron (ENCSR109RIQ)


title: DNase-seq from HCT116 (ENCSR498JAW)


title: DNase-seq from spleen (ENCSR097TGW)


title: DNase-seq from frontal cortex (ENCSR671GNH)


title: DNase-seq from HCT116 (ENCSR477IQW)


title: DNase-seq from gastrocnemius (ENCSR092QSI)


title: DNase-seq from cerebellum (ENCSR088WAL)


title: DNase-seq from ovary (ENCSR087SUF)


title: ATAC-seq from upper lobe of left lung (ENCSR895SEG)


title: ATAC-seq from posterior vena cava (ENCSR913FZQ)

summary:
ATAC-seq on human posterior vena cava

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: DNase-seq from cerebellum (ENCSR671GDA)


title: DNase-seq from left cerebral cortex (ENCSR084EBB)


title: ATAC-seq from heart left ventricle (ENCSR899YEP)


title: DNase-seq from thymus (ENCSR090RLB)


title: DNase-seq from HCT116 (ENCSR878VJL)


title: DNase-seq from urinary bladder (ENCSR885XDO)


title: DNase-seq from left cerebral cortex (ENCSR078JJT)


title: DNase-seq from adrenal gland (ENCSR667KPL)


title: ATAC-seq from ovary (ENCSR476WNA)

summary:
ATAC-seq on human ovary

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: DNase-seq from thymus (ENCSR068MCK)


title: DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR068KDQ)


title: ATAC-seq from fallopian tube (ENCSR238VHV)

summary:
ATAC-seq on human fallopian tube

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: DNase-seq from gastrocnemius (ENCSR073YXT)


title: DNase-seq from spleen (ENCSR876YAF)


title: DNase-seq from adrenal gland (ENCSR655MEK)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR875IVR)


title: DNase-seq from T-helper 2 cell (ENCSR655LUX)


title: DNase-seq from left cerebral cortex (ENCSR098GIZ)


title: DNase-seq from frontal cortex (ENCSR061TLH)


title: DNase-seq from immature natural killer cell (ENCSR654LST)


title: ATAC-seq from ovary (ENCSR872MAO)


title: DNase-seq from gastrocnemius (ENCSR119IUE)


title: DNase-seq from central memory CD4-positive, alpha-beta T cell (ENCSR467YCD)


title: DNase-seq from CD14-positive monocyte (ENCSR464ETX)


title: DNase-seq from layer of hippocampus (ENCSR459CXJ)


title: DNase-seq from thymus (ENCSR049ACM)


title: DNase-seq from kidney (ENCSR060ALG)


title: DNase-seq from left cerebral cortex (ENCSR471DVS)


title: DNase-seq from HCT116 (ENCSR867ITQ)


title: ATAC-seq from stimulated activated naive CD8-positive, alpha-beta T cell (ENCSR863TVR)


title: DNase-seq from urinary bladder (ENCSR453OSR)


title: DNase-seq from CD4-positive, alpha-beta memory T cell (ENCSR862ZDV)


title: DNase-seq from spleen (ENCSR039FQF)


title: ATAC-seq from fallopian tube (ENCSR565DSD)


title: DNase-seq from gastrocnemius (ENCSR862OIS)


title: DNase-seq from layer of hippocampus (ENCSR648GZU)


title: ATAC-seq from bile duct (ENCSR653ZWW)

summary:
ATAC-seq on human bile duct

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: ATAC-seq from T-cell (ENCSR032MEH)


title: ATAC-seq from heart left ventricle (ENCSR451JSB)


title: DNase-seq from gastrocnemius (ENCSR641XZF)


title: DNase-seq from cerebellum (ENCSR639CNY)


title: DNase-seq from CD4-positive, alpha-beta memory T cell (ENCSR437PXY)


title: DNase-seq from gastrocnemius (ENCSR854SEB)


title: DNase-seq from heart (ENCSR441MWY)


title: DNase-seq from lung (ENCSR427LHI)


title: DNase-seq from urinary bladder (ENCSR854UWF)


title: ATAC-seq from heart left ventricle (ENCSR848TMJ)


title: ATAC-seq from K562 (ENCSR859USB)

summary:
ATAC-seq on K562 cells stained for GATA1 and sorted for lowest 15% of expression

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: DNase-seq from left cerebral cortex (ENCSR636QXK)


title: DNase-seq from right cerebral cortex (ENCSR415MMR)


title: ATAC-seq from CD4-positive, alpha-beta T cell (ENCSR841LHT)


title: DNase-seq from thymus (ENCSR830IOW)


title: DNase-seq from left cerebral cortex (ENCSR029GTO)


title: DNase-seq from layer of hippocampus (ENCSR021NVL)


title: DNase-seq from adrenal gland (ENCSR632BLV)


title: DNase-seq from adrenal gland (ENCSR822RKU)


title: DNase-seq from heart (ENCSR021LAC)


title: DNase-seq from activated T-helper 1 cell (ENCSR636DIR)


title: ATAC-seq from jejunum (ENCSR415LEB)

summary:
ATAC-seq on human jejunum

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: ATAC-seq from posterior vena cava (ENCSR213DBU)


title: ATAC-seq from right cardiac atrium (ENCSR822BAD)

summary:
ATAC-seq on human right cardiac atrium

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: DNase-seq from natural killer cell (ENCSR409ZBD)


title: DNase-seq from lung (ENCSR211TTY)


title: DNase-seq from adrenal gland (ENCSR406JCQ)


title: ATAC-seq from effector memory CD8-positive, alpha-beta T cell (ENCSR019XCN)


title: DNase-seq from osteocyte (ENCSR818HHN)


title: ATAC-seq from sciatic nerve (ENCSR619LHF)

summary:
ATAC-seq on human sciatic nerve

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: DNase-seq from lung (ENCSR408JZW)


title: DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR614NSH)


title: DNase-seq from mammary epithelial cell (ENCSR817ALC)


title: DNase-seq from heart (ENCSR613LJB)


title: ATAC-seq from ureter (ENCSR814RGG)

summary:
ATAC-seq on human ureter

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: DNase-seq from stimulated activated naive CD8-positive, alpha-beta T cell (ENCSR208YDK)


title: DNase-seq from frontal cortex (ENCSR611CEJ)


title: ATAC-seq from heart right ventricle (ENCSR403GBR)


title: DNase-seq from right cerebral cortex (ENCSR017TAB)


title: ATAC-seq from heart left ventricle (ENCSR204PZT)


title: DNase-seq from HCT116 (ENCSR811COL)


title: DNase-seq from kidney (ENCSR018FXD)


title: DNase-seq from naive B cell (ENCSR017SBI)


title: DNase-seq from urinary bladder (ENCSR609SJP)


title: ATAC-seq from T-helper 17 cell (ENCSR803FKU)


title: DNase-seq from immature natural killer cell (ENCSR012RCX)


title: DNase-seq from inflammatory macrophage (ENCSR803BLT)


title: DNase-seq from naive B cell (ENCSR011VHK)


title: DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR400YJR)


title: DNase-seq from left cerebral cortex (ENCSR200TAZ)


title: DNase-seq from kidney (ENCSR605PMM)


title: DNase-seq from heart (ENCSR800YHA)


title: DNase-seq from stimulated activated naive CD8-positive, alpha-beta T cell (ENCSR009MDC)


title: TF ChIP-seq from K562 (ENCSR849LXI)

summary:
eGFP-MTF1 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: Cuspal shape alterations by Bmp4 directing cell proliferation and apoptosis

city: Seoul

first: Han-Sung

last: Jung

address: 50, Yonsei-ro, Seodaemun-gu

department: Dental School

country: South Korea

institute: Yonsei University

type: Expression profiling by high throughput sequencing

summary: To investigate the involvement of cuspal patterning with cell proliferation and apoptotic pathway, we compared gene expression profiling between mouse and gerbil tooth germs.

sample_organism:
Meriones unguiculatus
Mus musculus

platform_organism:
Meriones unguiculatus
Mus musculus

overall_design: Comparative gene expression profiling analysis of RNA-seq data in enamel knot region between mouse and gerbil during tooth development

first: Eun-Jung

last: Kim


title: Sequencing of yeast mutants

city: Salt Lake City

first: Jordan

middle: A

last: Berg

state: UT

address: 15 N Medical Drive East, Rm 5520

department: Biochemistry

institute: University of Utah

summary: Different yeast mutants with high mitochondrial membrane potential.

overall_design: RNA-seq (3 replicates of WT, mct1, sit4, sit4mct1, reg1, reg1mct1, sit4snf1, sit4snf1mct1, reg1snf1, reg1snf1mct1 from yeast)

first: Yeyun

last: Ouyang

first: Opal

last: Allen

first: Jared

last: Rutter


title: Analysis of physiological and miRNA-mRNA responses in the liver of crucian carp reveals its tolerance to hypoxia stress

status: Public on Oct 15 2022

city: lanzhou

first: jinqiang

last: huang

address: yintanlu stress

country: China

institute: Gansu Agricultural University

summary: Hypoxia has become one of the most critical factors limiting the development of aquaculture. Crucian carp (Carassius auratus) is widely consumed fish in China, with excellent tolerance to hypoxic environment. However, the molecular mechanisms underlying hypoxia adaptation and tolerance in crucian carp remain unclear. In this study, we detected the changes of biochemical parameters after hypoxia stress (3 h (H3h), H12h, and H24h) and reoxygenation (reoxygenation for 3 h after hypoxia 24 h (R3h)), mRNA and miRNA expression profiles under H12h compared to the control, and key hypoxia-related genes expression patterns in the liver of crucian carp through biochemical methods, RNA-seq, and qRT-PCR. Compared with the control, increased T-SOD, CAT, GSH-Px, T-AOC, ALT, and AST activities and MDA, TCHO, and TG contents, and decreased TP and ATP contents were observed after hypoxia stress, and LDH activity increased only in the H12h and H24h groups. Based on RNA-seq, 2479 differentially expressed (DE) mRNAs and 60 DE miRNAs were identified, and numerous DE mRNAs involved in HIF signaling pathway (hif-1α, epo, vegfa, and ho), anaerobic metabolism (hk1/hk2, pfk, gapdh, pk, and ldh) and immune response (nlrc3, nlrp12, cxcr1, cxcr4, ccr9, and cxcl12) were significantly upregulated after hypoxia exposure. Integrated analysis found that ho, igfbp1, hsp70, and hk2 were predicted to be regulated by novel_867, dre-miR-125c-3p/novel_173, dre-miR-181b-5p, and dre-miR-338-5p/dre-miR-128-3p, respectively, and targets of DE miRNAs were significantly enriched in MAPK signaling pathway, FoxO signaling pathway, glycolysis/gluconeogenesis, insulin signaling pathway, NOD−like receptor signaling pathway, and cytokine-cytokine receptor interaction. Expression analysis showed that the mRNA levels of vegfa, epo, ho, hsp70, hsp90aa.1, igfbp1, ldh, hk1, pfk, pk, and gapdh exhibited a remarkable increase, whereas sdh and mdh were downregulated in the H3h, H12h, and H24h groups compared with the control. These results contribute to our understanding of the molecular mechanisms of hypoxia tolerance in crucian carp, which are of great significance for genetics and breeding of other fishes tolerant to hypoxia.

first: Jinqiang

last: Huang

first: Shenji

last: Wu


title: Reconstitution of human adrenocortical specification and steroidogenesis using induced pluripotent stem cells [scATAC-seq]

city: Yiwu

first: keren

last: cheng

state: Zhejiang

address: 1575 chouzhou bei road

department: School of Medicine

institute: Zhejiang University

summary: The adrenal cortex produces vital steroid hormones that maintain homeostasis. While steroid hormones produced from the fetal zone adrenal cortex are essential for both fetal development and maintenance of pregnancy, the molecular mechanisms leading to human adrenal cortex development and steroid synthesis remain poorly understood due to the paucity of model systems. Through progressive generation of fetal zone adrenal cortex-like cells (FZLCs) from human induced pluripotent stem cells through posterior intermediate mesoderm-like, adrenogenic coelomic epithelium and adrenal primordium-like states, we provide the first in vitro reconstitution of human adrenocortical fetal specification. Generation of FZLCs faithfully recapitulates human embryonic adrenal cortex specification as evidenced by histomorphological and ultrastructural analysis, transcriptional profiles and delta-5 steroid biosynthesis and occurs in an adrenocorticotropic hormone (ACTH)-independent manner, consistent with clinical observations.  Furthermore, we demonstrate that FZLC generation is promoted by SHH and inhibited by NOTCH, ACTIVIN and WNT signaling and that steroid synthesis is amplified by ACTH/PKA signaling and blocked by pharmacologic inhibitors of delta 5 steroid synthesis enzymes. Finally, NR5A1 appear to self-stabilize its promoter activity and promote FZLC survival and steroidogenesis. Together, these findings provide a framework for understanding and reconstituting human adrenocortical development in vitro and pave the way for future cell-based therapies of adrenal insufficiency.

overall_design: scATAC-seq

first: Keren

last: Cheng

first: Yuka

last: Sakata

first: Michinori

last: Mayama

first: Kotaro

last: Sasaki


title: Reconstitution of human adrenocortical specification and steroidogenesis using induced pluripotent stem cells [scRNA-seq]

overall_design: scRNA-seq


title: Cell type- and region-specific transcriptome of an MPTP-induced mouse model of Parkinson’s disease

city: Guangzhou

first: Shanshan

last: Ma

state: Guangdong Province

address: No. 74 Zhongshan Road 2, Yuexiu District

institute: Sun Yat-sen University (North Campus)

summary: Aiming to gain brain region- and cell type-specific resolution in gene expression profiling during PD pathogenesis, we applied the translating ribosome affinity purification (TRAP) technique to enrich the ribosome-bound mRNA of DaNs, microglia and astrocyte, for RNA-Seq and analysis in a mouse MPTP model of PD.

overall_design: We performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells at two regions.

first: Congmin

last: Chen


title: Reconstitution of human adrenocortical specification and steroidogenesis using induced pluripotent stem cells

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

overall_design: Refer to individual Series


title: Effect of TGFB1 and Smad3 deficiency on doxorubicin cardiotoxity

city: Kansas City

first: Eugene

last: Konorev

state: MISSOURI

address: 1750 Independence Ave

department: Basic Sciences

institute: Kansas City University

summary: To examine the role of the TGF-beta/Smad3 pathway in cardiac damage by doxorubicin, we performed comparitive  RNA sequencing analysis of human cardiac endothelial cells transfected with  Smad3 shRNA

overall_design: To determine if the endothelial response to TGF-beta1 was enhanced by pretreatment with doxorubicin, human cardiac endothelial cells were pretreated with doxorubicin and subsequently exposed to TGF-beta1 to examine activation of the canonical pathway.

first: Katherine

last: Shortt

first: Daniel

middle: P

last: Heruth


title: Reconstitution of human adrenocortical specification and steroidogenesis using induced pluripotent stem cells [bulk RNA-seq]

overall_design: The following samples were prepared: fl0 hiPSC (WGNT SV20-211 [male, n =2]), aggregates at fl9 (whole WG+ fraction, WGNT SV20-211 [n=2]), fl14 (NT+ fraction, WGNT SV20-211 [n=2]), fl22 (NT+ fraction, WGNT SV20-211 [n=2]), fl22 (NT+ fraction, NT 312-2121 [female, n=2]), fl22 (NT+ fraction, WGNT SV20-KIKO19 [male, n=2]), ali21 (NT+ fraction, WGNT SV20-211 [n=1]), ali21 (NT+ fraction, NT 1390G-2125 [n=1]) and ali 28 (NT+ fraction, WGNT SV20-211 [n=1]), two human fetal stage (9 wpf) adrenal sample, one human fetal stage (9 wpf) heart sample.


title: Effect of Smad3 knockout on doxorubicin cardiotoxity

summary: To examine the role of the TGF-beta/Smad3 pathway in cardiac damage by doxorubicin, we performed comparitive  RNA sequencing analysis of cardiac endothelial cells isolated from WT and  Smad3 knockout mice.

overall_design: Experimental male mice utilized in the study received one or four weekly tail vein injections of doxorubicin, 5 mg/kg each, starting at 7 weeks of age. Control mice were injected with saline. Cardiac endothelial cells were isolated from mice treated with doxorubicin or saline 9 weeks after the last injection. RNA sequencing analysis was performed on the isolated cells.


title: Foxp3 expression diversifies the metabolic capacity and enhances the efficacy of CD8 T cells in adoptive T cell therapy

city: Pamplona

first: Enrique

last: Conde-Gallastegi

address: Av. de Pío XII, 55

country: Spain

institute: CIMA Universidad de Navarra

summary: CD4 regulatory T cells overwhelm conventional T cells in the tumor microenvironment (TME) thanks to a Foxp3-driven metabolic program that allows them to use alternate substrate and engage different metabolic pathways. In this study, we proposed to overexpress Foxp3 in CD8 T cells (CTL) and examine how it affected their antitumor properties. We show that Foxp3 overexpressing (Foxp3UP) CTLs proliferated and markedly accumulated in the TME while showing enhanced cytotoxicity and antitumor efficacy but not suppressor activity. Interestingly, tumor-infiltrating Foxp3UP CTLs exhibited a T-cell effector and leukocyte migration genetic signature, and positive enrichment in glycolysis, fatty acid (FA) metabolism and oxidative phosphorylation (OXPHOS) pathways. Intratumoral Foxp3UP CTLs showed an increased expression of Glut1, enhanced glucose and FA uptake and intracellular lipid accumulation. Interestingly, Foxp3UP CTLs compensated for the loss of mitochondrial respiration-driven ATP production by activating aerobic glycolysis. Moreover, in limiting nutrient conditions these cells engaged FA oxidation to drive OXPHOS for their energetic demands. Further, their ability to couple glycolysis and OXPHOS allowed then to sustain proliferation under glucose restriction. Our findings demonstrate a hitherto unknown role of Foxp3 in the adaptation of CTLs to TME that can be used to enhance their efficacy in adoptive T cell therapy

overall_design: Tumor bearing mice were treated with a mix of Foxp3UP and Mock CD8 T cells. After 5 days of treatment tumor cell suspensions containing transferred CTLs were surface stained with mAbs against distinctive population biomarkers (CD8, CD45.1 and/or CD90.1) in the presence of purified anti-CD16/32 mAb (Fc Block) and then with SYTOX Blue dead dye. Sorting of CTL subsets was performed in MoFloAstrio EQ (Beckman-coulter). RNA from transferred CD8 T cells was isolated using Maxwell 16 LEV simplyRNA tissue kit (Promega) and RNA libraries were prepared for sequencing using standard Illumina protocols.

first: S

last: Hervás-Stubbs

first: E


title: Mucociliary epidermis RNA-seq data from controls during early patterning (st. 9-12.5)

city: Freiburg

first: Peter

last: Walentek

state: BW

address: Breisacherstr. 113

department: Internal Medicine IV & IMITATE

country: Germany

institute: University Freiburg Medical Center

summary: This study was conducted to investigate the temporal expression of patterning genes in the Xenopus mucociliary epidermis.

overall_design:
Unmanipulated embryos were used to generate animal cap explants at embryonic stage 8. Explants were grown into mucociliary organoids and collected at embryonic stages 9, 10.5, 11.5, and 12.5 for total RNA extraction.

Please note that the DESeq2_result_*.tabular files have the following data columns:
GeneID, Base mean, log2(FC), StdErr, Wald-Stats, P-value, P-adj

first: Magdalena

last: Brislinger-Engelhardt


title: Blood transcriptome responses to PFOA and GenX treatment in the marsupial biomedical model Monodelphis domestica

city: Auburn University

first: Xu

last: Wang

state: AL

address: 273 CASIC Building, Auburn Research Park, 559 Devall Dr

department: Pathobiology, College of Veterinary Medicine

institute: Auburn University

summary: The objective of our study is to investigate the effect of PFOA and GenX on the gene expression levels in Monodelphis domestica whole blood cultures by RNA-seq and identify the major susceptible genes. We identified 578 differentially expressed genes (DEGs) in the PFOA treatment group and 148 DEGs in the GenX treatment group. 10 genes were selected for qRT-PCR validation and were confirmed to be DEGs. Pathway enrichment analysis revealed that several developmental processes were altered after PFOA exposure and showed an up-regulated pattern. And down-regulated DEGs after PFOA exposure were enriched for metabolic process and immune system process. GenX exposure is associated with up-regulated fatty acid transport pathways and inflammatory process. Our study is the first one to investigate the effects of PFASs on marsupial animals, providing supportive evidence of the similar transcriptomic alterations caused by PFOA and a fluorinated alternative GenX, which can work as a complement of the previous studies of PFASs effects on rodent or human.

overall_design: Monodelphis domestica (LSD strain) whole blood culture samples under PFOA treatment (n=4) and GenX treatment (n=2) compared to control samples (n=4). Monodelphis domestica (LSD strain) whole blood culture samples in 5 timepoints (0h, 12h, 24h, 48h, 72h) without treatment (n=14).

first: Wenqi

last: Cao


title: RNAi-mediated ablation of Nrf2 in PyMT-1099 LT, Py2T LT and MT∆Ecad mesenchymal breast cancer cells

city: Basel

first: Ravi Kiran Reddy

last: KALATHUR

state: Basel

address: Mattenstrasse 28

department: Departement Biomedizin

country: Switzerland

institute: University of Basel

summary:
Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. We have aimed at exploring the crosstalk between ROS  and an EMT induced by TGFb in breast cancer cells.
Methods: We observed that cells exposed to TGFb displayed a decrease of ROS levels. Furthermore, we identified an activation of the Nrf2 transcription factor, master regulator of the antioxidant response in TGFb-induced mesenchymal cells. In order to know the effect of Nrf2 ablation in epithelial and mesenchymal cells, RNAi-mediated ablation for Nrf2 was performed.
Results: RNAi-mediated ablation of Nrf2 led to mesenchymal cancer cell death due to ferroptosis, an iron- and oxidative stress-dependent cell death. Moreover, analysis revealed that several glutathione pathway genes were specifically regulated by Nrf2, suggesting a role of glutathione-related pathways in mesenchymal cell survival.
Conclusion: In this study we report the criticial role of the Nrf2-mediated glutathione metabolism in the protection of metastatic breast cancer cells from ferroptosis. Therapeutic targeting of antioxidant pathways may thus be beneficial for patients with metastatic disease.

overall_design: RNA-Seq of Py2T-1099 LT, Py2T LT and MT∆Ecad mesenchymal cells after RNAi-mediated ablation of Nrf2 performed in biological duplicates

first: Agathe

last: Morand

first: Ravi

middle: K

last: Kalathur

first: Gerhard

last: Christofori


title: Expression data from KKAy mice ileum tissue treated with voglibose

city: Beijing

first: 唐

last: 伟评

address: 2 Anzhen Rd, Chaoyang District,

institute: Beijing Institute of Heart Lung and Blood Vessel Diseases

summary:
Voglibose is an α-glycosidase inhibitor with anti-inflammatory effects on the intestine, but the underlying mechanism is not clear. Our study defined the dynamic changes of the differentially expressed genes after treatment of voglibose in diabetic KKAy mice, and provide basis for comprehensive understanding of the disease at molecular level.
We investigated gene expression alteration after a long-term treatment of voglibose in diabetic KKAy mice.

overall_design: After feeding for 4 weeks of high-fat diets, KKAy mice were treated intragastrically with Voglibose (1mg/kg) or an equivalent volume of water (0.05 ml/10 g body weight) once daily for 8 weeks. Total RNA was extracted from ileum tissues using Trizol reagent (Life Technologies, Carlsbad, CA, USA) (n=4 per group) according to manufacturer’s instructions. All arrays were scanned by using Affymetrix® GeneChip Command Console (AGCC) which was installed in GeneChip® Scanner 3000 7G. A total of 2,2207 detectable effective genes were obtained and 1528 genes were significantly differentially expressed genes (fold change > 1.2, p < 0.05) between the voglibose-treated group and the DM group, of which 603 were upregu-lated and 925 were downregulated.

first: Shuai-Nan

last: Liu

first: Ya-Xin

last: Fu


title: A Potential Diagnostic Biomarker in Pulmonary Hypertension

status: Public on Oct 14 2022

city: ChangSha

first: Ke

last: Gong

address: 139 Renmin Middle road

department: cardiovascular surgery

institute: The Second Xiangya Hospital of Central South University

summary: Right heart failure results from advanced pulmonary hypertension (PH) and has a poor prognosis. There are few available treatments for right heart failure. Pulmonary artery remodeling, including changes in pulmonary artery endothelial cells to endothelial-mesenchymal cells, and aberrant fibroblast and pulmonary artery smooth muscle cell (PASMC) proliferation, are characteristics of the pathophysiological process of PH. As a result, the clinical situation requires novel PH diagnostic and treatment targets.

overall_design: Monocrotaline was used to create an animal model of PH, and lung tissue was removed for transcriptome sequencing. The targets with the highest differences were chosen for transfection after possible targets were identified using bioinformatic techniques and confirmed by qPCR to examine their function in hypoxic PASMCs.


title: Expression profiling of lung endothelial cells from control and nANGPTL4 AAV treated mice.

city: Heidelberg

first: Ashik Ahmed

last: Abdul Pari

address: Im neuenheimer Feld 280

institute: German Cabcer Research Institute

summary: Lung EC were isolated from control and nANGPTL4 AAV treated mice and bulk RNA-seq analysis was performed.

overall_design: Total RNA-sequencing of FACS-sorted lung endothelial cells was undertaken. Four independent biological replicates for each condition were analyzed.

first: Corinne

last: Hubers

first: Hellmut

middle: G

last: Augustin

first: Moritz

last: Felcht


title: Py2T C40 and Py2T I60 cells, long-term treated murine derived breast cancer cell lines with H2O2

summary:
Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. We have aimed at exploring the crosstalk between ROS  and an EMT induced by TGFb in breast cancer cells.
Methods: We observed that cells exposed to TGFb displayed a decrease of ROS levels. To identify the antioxidant pathways activated during EMT, we investigated the effect of long-term oxidative stress, for example by H2O2 (40 µM and 60 µM), on Py2T epithelial cells derived from the MMTV-PyMT mouse model.
Results: We show that long-term treated Py2T epithelical cells with H2O2 display both higher migratory capability and tumorigenicity. Furthermore, we identified an activation of the Nrf2 transcription factor, master regulator of the antioxidant response, in H2O2-resistant cells, as well as in TGFb-induced mesenchymal cells.
Conclusion: In this study we report the criticial role of the Nrf2-mediated glutathione metabolism in the protection of metastatic breast cancer cells from ferroptosis. Therapeutic targeting of antioxidant pathways may thus be beneficial for patients with metastatic disease.

overall_design: RNA-Seq of H2O2 Py2T cells (Py2T C40 and Py2T I60) performed in biological duplicates


title: MTflEcad I80 and MTflEcad DI150 cells, long-term treated murine derived breast cancer cell lines with H2O2

summary:
Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. We have aimed at exploring the crosstalk between ROS  and an EMT induced by TGFb in breast cancer cells.
Methods: We observed that cells exposed to TGFb displayed a decrease of ROS levels. To identify the antioxidant pathways activated during EMT, we investigated the effect of long-term oxidative stress, for example by H2O2 (80 µM and 150 µM), on MTflECad epithelial cells derived from the MMTV-Neu mouse model.
Results: We show that long-term treated MTflEcad epithelical cells with H2O2 display both higher migratory capability and tumorigenicity. Furthermore, we identified an activation of the Nrf2 transcription factor, master regulator of the antioxidant response, in H2O2-resistant cells, as well as in TGFb-induced mesenchymal cells.
Conclusion: In this study we report the criticial role of the Nrf2-mediated glutathione metabolism in the protection of metastatic breast cancer cells from ferroptosis. Therapeutic targeting of antioxidant pathways may thus be beneficial for patients with metastatic disease.

overall_design: RNA-Seq of H2O2 MTflEcad cells (MTflEcad I80 andMTflEcad DI150) performed in biological duplicates


title: Genome-wide identification of Foxf2 transcriptional target genes in tongue development

city: Cincinnati

first: Jingyue

last: Xu

state: OH

address: 3333 Burnet Ave

department: Developmental Biology

institute: Cincinnati Children's Hospital

summary: The tongue is a specialized muscular organ that performs multiple essential functions including mastication, deglutition, oral sensation, oral cleansing, airway maintenance and vocalization. In this study, we show Foxf1/Foxf2 serves as key mediators of hedgehog signaling in regulating myoblast migration, differentiation, and intrinsic tongue muscle organization. We took advantage of the Foxf2FLAG mice which carries 3xFLAG epitope-tagged endogenous Foxf2 protein and characterized genome-wide Foxf2 binding sites in the developing tongues using chromatin immunoprecipitation and genome sequencing (ChIP-seq). Further analyses demonstrate that Foxf1/2 transcription factors directly control the expression of Hgf, Tgfb2, and Tgfb3, to regulate tongue myogenesis.

overall_design: We generated mice carrying 3xFLAG epitope-tagged endogenous Foxf2 protein using the CRISPR/Cas9-mediated genome editing technology. 75 tongue tissues were dissected from Foxf2FLAG/FLAG embryos at E12.5. ChIP was performed by using anti-FLAG antibodies (Sigma). Sequencing libraries were generated using ThruPLEX DNA sequencing kit (Takara). Sequencing was performed on an Illumina Nextseq500 (Illumina, San Diego CA). For ChIP-Seq data analysis, raw FASTQ files were aligned to mm10 reference genome using Bowtie2. Peak calling and de novo motif identification were performed using the HOMER (Hypergeometric Optimization of Motif EnRichment) software. The input samples were used as the control for calling peaks from the Foxf2-FLAG ChIP-seq data sets.

first: Rulang

last: Jiang


title: Intestinal epithelium P7 Maf DKO RNA-seq

city: Durham

first: Anne (Maggie)

middle: M

last: Bara

state: NC

address: 307 Research Dr.

department: Cell Biology and Dermatology

institute: Duke University

summary: To investigate the function of Maf family transcription factors, MafB and cMaf, in the intestinal epithelium, we generated tissue specific loss of function mouse models.

overall_design: VillinCre was used to drive deletion of transcription factors MafB and cMaf (MafBfl/fl, cMaf fl/fl) in the intestinal epithelium.  At postnatal day 7, intestines were collected, RNA was isolated and samples were sent to Novogene for library prep, sequencing and analysis.

first: Maggie

first: Terry

last: Lechler


title: ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.

city: New York City

first: Dan

last: Li

state: NY

department: HOPP

institute: Memorial Sloan-Kettering Cancer Center

summary: Comparision of transcriptome of PC3 and 22Rv1 prostate cell lines after 1 week overexpression of mutated ETV4: ETV4AAA-IRES-eGFP, wild type ETV4: ETV4WT-IRES-eGFP, and control vector IRES-eGFP by MSCV-IRES-GFP vector ((Addgene #20672)) and Lentivirus transduction.

overall_design: Alive prostate cells of of PC3 and 22Rv1 prostate cell lines after 1 week overexpression of mutated ETV4: ETV4AAA-IRES-eGFP, wild type ETV4: ETV4WT-IRES-eGFP, and control vector IRES-eGFP were isolated by Fluorescence-activated cell sorting (FACS) according to eGFP and DAPI and analyzed using RNAseq.

first: Yu

last: Chen


title: Sequencing of yeast mutants with or without phosphate depletion

first: Jordan

last: Berg

summary: Targeting of yeast with genetic or nutrient perturbation to assess mitochondrial membrane potential and its regulation.

overall_design: RNA-seq (3 replicates of WT, prototrophic WT, pho85, rpo41, or rpo41/pho85 deletion in yeast, and bar1 deletion in W303 yeast) in samples with or without depletion of phosphate, nitrogen, and/or uracil.

first: Yeyun

last: Ouyang

first: Jared

last: Rutter


title: MiRNA microarray of overexpression Ctrl and PRLR AsPC-1 cells.

city: Shanghai

first: YingNa

last: Liao

address: No. 25, Lane 2200, Xietu Road, Shanghai

institute: Shanghai Cancer institute

summary: The study is to explore differentially expressed miRNAs in AsPC-1 cells overexpressing Ctrl or PRLR.

overall_design: The miRNA microarrays were performed to investigate the differentially expressed miRNAs in PRLR-overexpressed AsPC-1 cells compared to control cells.Each group contains three biological replicates.

first: PeiQi

last: Huang


title: Characterization of a NEK7-related pyroptosis gene signature against pancreatic cancer and evaluation of its potential in tumor microenvironment remodeling via regulating inflammasome complex

city: Shenzhen

first: Jianhua

last: Qu

state: Guangdong

address: Lianhua Road 1120

institute: Peking University ShenZhen Hospital

summary: To investigate the biological function of NEK7 in pyroptosis of pancreatic cancer cells, we manipulate the expression of NEK7 and NEK6 in pancreatic cancer cell lines in which each target gene has been knocked down by siRNA.

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells. Comparative gene expression profiling analysis of RNA-seq data for CFPAC and KP3 cells.

first: Zilong

last: Yan


title: Identification of a serum 48-lncRNA signature as diagnostic marker for hepatocellular carcinoma and liver cirrhosis

first: Li-Si

last: Zeng

address: 651 Dongfeng Road East

department: Sun Yat-Sen University Cancer Center

institute: Sun Yat-Sen University

summary:
In cancer management, early and accurate diagnosis of hepatocellular carcinoma (HCC) is important for enhancing survival rate of patients. Currently, serum alpha-fetoprotein (AFP) is the only one biomarker for detection of HCC. However, serum AFP is not satisfactory for diagnosis of HCC due to its low accuracy (about 60-70%). In this study, we collected 109 serum samples (discovery set) from healthy control (HC) and patients with chronic hepatitis B (CHB), liver cirrhosis (LC) and HCC, and analyzed them with custom lncRNA microarray. Profiling analysis shows 181 differentially expressed lncRNAs between HCs and patients with CHB, LC and HCC. Then a 48-lncRNA diagnostic signature was identified with 100% predictive accuracy for all subjects in the discovery set. This diagnostic signature was verified with a cross-validation analysis in the discovery set. To further corroborate the signature, we gathered another 66 serum samples (validation set) and also analyzed them with microarray. The result indicates that the same signature has similar diagnostic accuracy for HC (100%), CHB (73%), LC (88%) and HCC (95%), implying a reproducible diagnostic biomarker for HCC. Receiver operating characteristic (ROC) analysis exhibits that this signature has significantly higher diagnostic accuracy for HCC and non-cancerous subjects (area under curve [AUC]: 0.994) than AFP (AUC: 0.773) in the discovery set and this was also verified in the validation set (0.964 vs 0.792). More importantly, the signature detected small HCC (<3cm) with 100% (13/13) accuracy while AFP with only 61.5% (8/13). Altogether, this study demonstrates that the serum 48-lncRNA signature is not only a powerful and sensitive biomarker for diagnosis of HCC but also a potential biomarker for LC.

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Submitter declares these data are subject to patent number ZL 2016 1 0397094.
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overall_design: In this study, we aimed to profile serum lncRNA expression and identify a signature for diagnosis of HCC. Firstly, we collected 109 serum samples (discovery set) from healthy control (HC) and patients with chronic hepatitis B (CHB), liver cirrhosis (LC) and HCC, and analyzed them with custom lncRNA microarray. To further corroborate the signature, we gathered another 66 serum samples (validation set) and also analyzed them with microarray.

first: Hui-Yun

last: Wang


title: Expression data of human NK cell treated with lenalidomide

city: Seongnam-si

first: KyuBum

last: Kwack

address: 335, Pangyo-ro, Bundang-gu

department: Institute Department of Biomedical Science

institute: College of Life Science, CHA University

summary: Lenalidomide, an analogue of thalidomide, is immuno-modulatory drug and has been used for many types of cancer therapy. Recently, it has been reported that lenalidomide can enhance the function of NK cell during IL-2 response. However, molecular mechanism of action of lenalidomide in NK cells is unclear still. To investigate the modification by lenalidomide on NK cells, we conducted the analysis of gene expression on NK cells.

overall_design: PBMCs were isolated from 2 healthy donors using by Ficoll-Hypaque density gradient centrifugation on Histopaque-1077 (Sigma-Aldrich). PBMCs were cultured with DMSO or 1uM lenalidomide plus 200U/ml IL-2 for 12 days. Human NK cell separated by NK cell isolation kit (Miltenyi Biotec) on day 12. NK cell purity was at least 85% and used for microarray analysis

first: JeongMin

last: Sim

first: YoungJoon

last: Park

first: JuWon

last: Ahn


title: Effect of subcutaneous fat (SF) loss on gene expression with clear cell renal cell carcinoma

city: Seoul

first: BYULA

last: JEE

address: 81 Irwon-Ro Gangnam-gu

department: Urology

institute: Samsung medical center

summary:
RCC is one of known malignancies in terms of the association between body mass index (BMI), adiposity, and prognosis, showing overall survival (OS) improvement in obese patients. Despite of increasing interest in this unexpected survival benefit of obesity, termed the “obesity paradox”, previous studies focused on the baseline features without considering their changes. Given that these changes, especially for rapid loss of adipose tissue, are also reported to have a prognostic value in cancer patients, and that ICI therapy can lead to substantial change in body composition, it may be reasonable to assume that these changes are also associated with patient prognoses. However, its prognostic impact on patients with metastatic ccRCC undergoing ICI therapy has not been established.
In this study,  We investigated the association between these changes and molecular features by targeted sequencing and RNA sequencing of tumor samples to understand the underlying biology.

overall_design: Comparative gene expression profiling analysis of RNA-seq data between ccRCC with delta SF0 and ccRCC with delta SF1

first: Minyoung

last: Kang


title: Seeking insights into early onset colorectal cancer through analysis of normal colon organoids of Familial Adenomatous Polyposis patients

status: Public on Oct 13 2022

city: Charlottesville

first: Matthew

last: Devall

state: Virginia

address: 1335 Lee Street

institute: University of Virginia

summary: Here, we generated bulk RNA-seq data on colon organoids derived from both healthy and familial adenomatous polyposis patients. We related findings observed within this dataset to differential expression findings from a publicly available colorectal cancer cohort.

overall_design: Analysis of the effects of carcinogen treatment on gene expression in colon organoids

first: Casey

last: Graham

first: Li

last: Li

first: Devall

last: Matthew


title: Swc4 protects nucleosome free chromatin of telomeres, tRNA genes and rDNA loci to inhibit genome instability [ChIP-Seq]

first: Yue

last: Pan

address: 320 Yue Yang Road

department: Center for Excellence in Molecular Cell Science, CAS

institute: Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences

summary: In the baker’s yeast Saccharomyces cerevisiae, Swc4, Yaf9, Arp4, and Act1 form a submodule shared by histone acetylation NuA4 complex and chromatin remodeling SWR1 complex (SWR1-C). Act1 and Arp4 are essential for cell survival. Deletion of SWC4, but not YAF9, results in severe growth defect, however, the underlying mechanism remains largely unknown. Here, we show that swc4Δ, but not yaf9Δ, eaf1Δ, or swr1Δ cells display mitotic defects in both faithful chromosome segregation and DNA ploidy, suggesting that the defects observed in swc4Δ cells are independent of the integrity of either NuA4 or SWR1-C. Additionally, loss of Swc4 function results in chromosomal breakage and spindle assembly check-point activation. Swc4 binds to telomeres, tRNA and rDNA regions in genome, which represent nucleosome free regions (NFRs) of chromatin. Notably, telomeres, tRNA genes and rDNA loci, in swc4Δ cells become unstable and are highly susceptible to recombination. Taking together, we conclude that the chromatin associated Swc4 protects nucleosome-free chromatin from breakage to ensure genome integrity.

overall_design: Examination of the enrichment of myc tagged Swc4 on chromatin in the budding yeast

first: Jia-Cheng

last: Liu

first: Yu-Long

last: Chen

first: Lin-Jun

last: Hou

first: Jin-Qiu

last: Zhou


title: The Arf‐GAP Proteins AoAge1 and AoAge2 are Required for Mycelial Growth, Conidiation, Stress Responses, Trap Formation, and the Secondary Metabolism in the Nematode-Trapping Fungus Arthrobotrys oligospora

city: Kunming

first: yang

last: le

address: No.2 of Cuihubeilu

institute: Yunnan university

summary: ADP-ribosylation factors (Arfs) belong to the small GTPases superfamily and regulate mycelial development, endocytosis, and virulence in fungi. Nematode-trapping (NT) fungi can form unique infection structures (traps) to capture and kill free-living nematodes, thus play a potential role in the biocontrol of nematodes. Arthrobotrys oligospora is a representative species of the NT fungi. Here, the functions of two Arf-GAPs, Age1 (AoAge1) and Age2 (AoAge2) orthologue to S. cerevisiae were identified in A. oligospora by gene knockout and multi-phenotypic analysis. It was found that AoAge1 and AoAge2, especially AoAge2, play an important role in vegetative growth, conidiation, trap formation, DNA damage, endoplasmic reticulum stress, mitochondrial activity, endocytosis, heat shock stress, ROS level, and autophagy of A. oligospora. Importantly, our transcriptomic analysis (12 h) showed that nearly 62.7% of A. oligospora genes (11479) were directly or indirectly regulated by AoAge2, indicating that Arf-GAP plays a global role in the growth and development of A. oli gospora.   Revealed by transcriptomic analysis differentially upregulated genes in the absence of Aoage2 were involved in autophagy and carbohydrate, amino acid and sphingolipid metabolism while downregulated genes were involved in longevity regulating pathway and carbohydrate, amino acid and secondary metabolites biosynthesis. In addition, metabolomic analysis showed that many compounds were markedly reduction in ΔAoage2 mutants strain. Our results highlighted that AoAge1 and AoAge2 play a crucial role in the asexual growth, development, differentiation, and lifestyle transition, especially, AoAge2 is indispensable for conidiation and trap morphogenesis of A. oligospora. These results demonstrated crucial roles for AoAge1 and AoAge2 in the fungal growth, environmental adaption and pathogenicity, which provided insights into the function of Arf-GAPs in A. oligospora and other fungi.

overall_design: Mycelial samples of the WT and ΔAoage2 mutant strains were collected after trap formation induced by nematodes at different time points (0, 6, 12, and 24 h), and cDNA libraries of each sample were constructed and sequenced.

first: Le

last: Yang

first: Xuemei

first: Yuxin

last: Ma

first: Meichen

last: Zhu

first: Keqing

last: Zhang

first: Jinkui


title: NASH treatment study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

city: Corvallis

first: Andrey

last: Morgun

state: Oregon

address: Pharmacy Building, 1601 SW Jefferson Way

department: College of Pharmacy

institute: Oregon State University

summary: Mice on a reference (RD) or western diet (WD) supplemented with olive oil or the omega-3 fatty acid docosahexaenoic acid DHA

overall_design: 24 samples, 5-7 replicates per treatment, including a control (RD), a WD (baseline, WDB), a western diet with olive oil (WDO) and a WD with DHA treatment (WDD)

first: Donald

last: Jump

first: Natalia

last: Shulzhenko


title: Genome-scale CRISPR screen identifies nucleotide metabolism as an actionable therapeutic vulnerability in diffuse large B-cell lymphoma [RNA-seq]

city: Tabuk

first: Sael

last: Alatawi

address: Duba Road

country: Saudi Arabia

institute: University of Tabuk

summary: Myc dysregulation underpins lymphomagenesis in the Atm-null DLBCL model and confers dependence on nucleotide biosynthesis.MYC-driven DLBCL is sensitive to nucleotide depletion with combined mycophenolate mofetil and adavosertib in vitro and in vivo.

overall_design: Eleven biological replicates were analyzed for ATM-null and two biological replicates for the control (ATM wild type)


title: NASH prevention study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

summary: Mice on a reference (RD) or western diet (WD) supplemented with olive oil or omega-3 fatty acids (eicosapentaenoic acid [EPA] and/or docosahexaenoic acid [DHA])

overall_design: 40 samples, 8 replicates per treatment, including a control, a WD without treatment, and a WD with treatments


title: Total RNAseq of Lactobacillus fermentum

city: Taipei

first: Hsu-Feng

last: Chu

address: No.155, Sec.2, Linong Street

country: Taiwan

summary: We applied total RNA sequencing of Lactobacillus fermentum strain GR1008 and GR1009 and compare the differentially expressed genes. This study aimed to find out the underlying mechanims for the differential morphology of the two strains.

overall_design: Comparative study of gene expression level of GR1008 and the morphotypic variant strain GR1009

first: Ching-Ting

last: Lin

first: Chien-Chen

last: Wu


title: Tissue-level dissection of obesity-exercise axis in adipose-muscle tissues

city: Boston

first: Jiekun

address: 32 Vassar Street

institute: MIT

summary: We studied the opposing effects of exercise training and high-fat diet at tissue-level resolution to reveal gene expression and pathway changes in subcutaneous white adipose tissue, visceral white adipose tissue, and skeletal muscle. We revealed gene modules consistently up-regulated by exercise training, which include fatty acid biosynthesis/beta-oxidation/metabolism, oxidative phosphorylation, TCA cycle, and ROS response. Modules down-regulated by exercise training in all three tissues are antigen presentation, neutrophil degranulation, immune cell migration, phagosome-related genes, ECM-related genes, proliferation, and ribonucleotide biosynthesis. Taken together, exercise training improves fatty acid metabolism and cellular respiration similarly across the three metabolic tissues, and represses immune, ECM, proliferation and tissue-specific pathways.

overall_design: Bulk mRNA profiles of three metabolic tissues from 6-week old C57BL/6JN mice with 6-week high-fat diet and 3-week exercise training interventions

first: Maria

last: Vamvini

first: Pasquale

last: Nigro

first: Laurie

last: Goodyear

first: Manolis

last: Kellis


title: Transcriptional profiling of striatum and cortex from a LacO-Q140 inducible mouse model of Huntington’s disease with early and late mutant HTT lowering

city: Princeton

first: Jeff

last: Aaronson

state: New Jersey

address: 155 Village Boulevard, Suite 200

department: Discovery & Systems Biology

institute: CHDI

summary: Inducible mutant huntingtin mice were genetically engineered by introducing the lac operon sequence (LacO) into the Q140 promoter of the Q140 KI mice. LacO-140Q mice were then crossed to transgenic Lac repressor protein (LacIR) mice. LacIR occupies the LacO sequence in the promoter and thereby blocks transcription of Q140. Beta-galactoside analog isopropyl thiogalactoside (IPTG) binds to LacIR, which results in decreased affinity between the repressor and operator, thereby relieving repression. All mice in this study have the LacIR transgene, therefore the default state of the mouse containing LacOQ140;LacIR is maximal repression of Q140. CHDI generated and analyzed RNASeq data from inducible LacOQ140 mice at 2 points: 6 and 12 months. Transcriptional profiling in the striatum and cortex with early versus late mutant HTT lowering is detailed.

overall_design: Hdh(LacO-140Q/+):β-actin-LacIR tg or Hdh(LacO-+/+):β-actin-LacIR tg wild-type mice received either no treatment or ОІ-D-1-Thiogalactopyranoside (IPTG) treatment starting at E5 and continued to 2 months or 8 months of age or throughout life. RNASeq analysis was performed on samples from the striatum and cortex at 6 and 12 months of age. N = 10 per group (5F/5M). There are 4 groups at 6 months of age and 5 groups at 12 months of age.

first: Jim

last: Rosinski


title: LX2 cell line treated with or without BTC, and with or without fatty acids (Oleic acid and Omega3), and subsequent gene expression

summary: LX2 cells treated with or without BTC and with or without oleic acid or DHA

overall_design: LX2 cells were obtained from SL Friedman (Mount Sani Medical School) (46). LX2 cells are activated human hepatic stellate cells; they were maintained in DMEM with 10% FCS containing penicillin and streptomycin. Cells were plated onto 100 mm plastic petri dishes ∼100,000 cells/plate and treated with fatty acids (at 50 μM) in endotoxin-free BSA (at 20 μM) during the growth phase. Fatty acids [oleic acid (18:1 ω9) and DHA (22:6, ω3); Nu-Chek Prep] were used at 50 μM for 2- 48-hour cycle treatments. After this pre-treatment, cells were trypsinized, washed in PBS, counted and plated at 3000 cells/well in a 96-well plate. Cells were fed DMEM with 1 % FCS without or with betacellulin (human recombinant betacellulin (BTC), R&D Systems) for 72 hrs; the concentration ranged from 1.25 to 25 ng/ml. At the completion of BTC treatment, media was removed, washed with PBS and DNA/well was quantified using the CyQuant cell proliferation assay (Thermofisher); DNA fluoresces was quantified [excitation at 485 nm & emission at 530 nm. This experiment was repeated 3 times.

first: Morgun

last: Andrey

first: Shulzhenko

last: Natalia

first: Jump

last: Donald


title: Expression data from actinic lentigines in European volunteers

city: Aulnay sous Bois

first: Emilie

last: Warrick

address: 1 avenue Eugène Schueller

country: France

institute: L'Oreal R&I

summary: Actinic lentigines (AL) are very common hyperpigmented lesions that develop on chronically sun-exposed skin and represent a visible sign of skin ageing. In this study, a homogeneous group of advanced AL lesions was selected using epiluminescence imaging and pigmented pattern scoring. Gene expression profiling was performed  on AL compared with adjacent non lesional (NL) skin.

overall_design: Thirteen European women aged 51-67 years, phototype II-III were included in the study. Pairs of 3-mm biopsies (AL lesion and adjacent NL skin) were obtained on the back of hands from each volunteer.

first: Christine

last: Duval

first: Françoise

last: Bernerd


title: THP-1 cell lines treated with or without BTC and TLR2/4 ligands, and their subsequent gene expression

first: Andrey

last: Morgun

summary: THP-1 cells treated with or without BTC and TLR2/4 ligands

overall_design: THP-1 monocytes were cultured in RPMI 1640 medium adjusted to contain 4.5 g/L glucose and supplemented with 1% Penicillin/Streptomycin, 10% FBS, 1 mM sodium pyruvate, 10 mM HEPES. For experiments, monocytes were first seeded in 24 well plates at 400,000 cells/well in 1 mL of complete medium with 50 ng/mL PMA (phorbol 12-myristate 13-acetate) to induce polarization, for 24 hours. Then, attached cells were washed with sterile PBS to remove residual serum and PMA containing media. Cells were stimulated with a TLR2 agonist at 40 ng/mL (PGN-BS, Invivogen, San Diego, CA), TLR4 agonist at 4 ng/mL (LPS-B5, Invivogen, San Diego, CA), BTC at 40 ng/mL (human recombinant Betacellulin protein, R&D systems, MN), or combinations of all for 6 hours. Treatments were prepared in serum-free semi-complete RPMI 1640 media (see above for other components) supplemented with 20 μM BSA and 50 μM BHT (Butylated hydroxytoluene). Cells were lysed with 300 μL RLT buffer (Qiagen) and cell lysates were stored at -80 ºC.

first: Natalia

last: Shulzhenko


title: Exploring the effect of electroacupuncture stimulation of Lung Meridian of Hand-Taiyin on synaptic plasticity in rats with cerebral ischemia-reperfusion injury based on Transcriptomics

city: Changsha

first: Kailin

last: Yang

state: Hunan

address: Xueshi Road No. 300

institute: Hunan University of Chinese Medicine

summary: Background: Electroacupuncture (EA) were progressively gained popularity in the treatment of neurological disorders such as ischaemic brain injury in recent years. But the therapeutic mechanisms of EA are yet not well addressed. This research aims to explore the effect of electroacupuncture stimulation of Lung Meridian of Hand-Taiyin on synaptic plasticity in rats with cerebral ischemia-reperfusion injury based on Transcriptomics  Methods: Rats were randomly divided into sham operation group, model group and EA group. Rats in the model group and the EA group were prepared for the middle cerebral artery occlusion/reperfusion (MCAO/R) model. In the EA group, the representative acupoints of the Lung Meridian of Hand-Taiyin (Tianfu acupoints, Chize acupoints, Kongzui acupoints and Taiyuan acupoints) were selected for electroacupuncture stimulation.  Transcriptomics was performed after the intervention.

overall_design: Comparative gene expression profiling analysis of RNA-seq data

first: Jiang

last: Pan

first: Hongwei

last: Shen

first: Wei

last: Zhang


title: Single-cell transcriptome Atlas reveals protective characteristics of COVID-19 mRNA vaccine [bulk RNA-seq]

status: Public on Oct 12 2022

first: Xingguang

last: Liu

address: Xiangyin road 800

department: National Key Laboratory of Immunity & Inflammation

institute: Naval medical university

summary: mRNA vaccines are promising alternatives to conventional vaccines in many aspects. We previously developed a lipopolyplex (LPP)-based mRNA vaccine (SW0123) that demonstrated robust immunogenicity and strong protective capacity against SARS-CoV-2 infection in both mice and rhesus macaques. However, the immune profiles and mechanisms of pulmonary protection induced by SW0123 remain unclear. Through high-resolution single cell analysis, we found that SW0123 vaccination effectively suppressed SARS-CoV-2-induced inflammatory responses by inhibiting the recruitment of pro-inflammatory macrophages and increasing the frequency of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). In addition, the apoptotic process in both lung epithelial and endothelial cells was significantly inhibited, which was proposed to be one major mechanism contributing to vaccine-induced lung protection. Cell-cell interaction in lung compartment was also altered by vaccination. These data collectively unraveled the mechanisms by which the SW0123 protects against lung damage caused by SARS-CoV-2 infection.  reduces cardiac function, leading to cardiac remodeling and heart failure. However, the early neonatal mice have a strong ability in cardiomyocyte proliferation and cardiac regeneration after heart damage such as apical resection. Besides of cardiomyocytes, non-myocytes in heart tissue also play important roles in the regeneration process. Previous studies showed that cardiac macrophages, regulatory T cells and CD4+ T cells are all involved in regulating the myocardial regeneration process. However, the roles of other cardiac immune cells in cardiac regeneration remains to be elucidated.  B cells is a prominent immune cell in injured heart; here we discovered the indispensable function of cardiac B cells in improving cardiomyocyte proliferation and heart regeneration in neonatal mice.

overall_design: Rhesus macaques received three doses of mRNA vaccine SW0123 or PBS. Then rhesus macaque were challenged by SARS-CoV-2 2 weeks after the last vaccination. The bronchoalveolar lavage fluid from rhesus amcaques were collected 1 week post SARS-CoV-2 infection.

first: Yong

last: Tan

first: Ang

last: Lin

first: Zhenzhen

last: Zhan


title: Effect of glucokinase regulatory protein (GCKR)-rs1260326 on gene expression  in human liver organoids

first: Kentaro

last: Iwasawa

address: 3333 BURNET AVENUE

department: Division of Gastroenterology, Hepatology and Nutrition

institute: Cincinnati Children's Hospital Medical Center

summary: To investigate the functional difference between rs1260326:C>T in the regulation of lipogenesis in the liver, we established human induced pluripotent stem cell lines from GCKR CC  and GCKR TT variants.

overall_design:
We then performed gene expression profiling analysis using data obtained from RNA-seq of human liver organoids (HLOs) generated from 5 different cell lines of which 2 are GCKR TT variants and 3 from GCKR CC variants
Comparative gene expression profiling analysis of RNA-seq data for human liver organoids generated from GCKR TT and CC cell lines.

first: Kimura

last: Masaki

first: Iwasawa

last: Kentaro

first: Takebe

last: Takanori


title: Single-cell dissection of obesity-exercise axis in adipose-muscle tissues

first: Jiekun

summary: We studied the opposing effects of exercise training and high-fat diet at single-cell resolution to reveal changes in cell type abundance, cell-type-specific gene expression/pathway/regulatory network changes, and changes in cell-cell communication both within and across tissues. We profiled scRNA-seq in 204,883 cells, grouped into 53 distinct cell sub-types/states across 22 major cell types, from subcutaneous white adipose tissue, visceral white adipose tissue, and skeletal muscle across 16 lean and 15 obese mice with both diet and exercise interventions. Changes in both cell proportion and transcriptional state were most strongly pronounced in adipose stem cells in fat, consistent with roles of adipogenesis in thermogenesis-vs-lipogenesis and hyperplasia-vs-hypertrophy in obesity. For immune cells, exercise training decreases obesity-associated inflammatory tissue-resident cell populations, including myeloid and regulatory T cells, and promotes beige-cell-inducing populations, including NKT cells. These changes clustered in common pathways across tissues for both exercise and obesity, including extracellular matrix remodelling and circadian rhythm in mesenchymal stem cells and cell activation/migration in immune cells.

overall_design: Single-cell mRNA profiles of three metabolic tissues from 6-week old C57BL/6JN mice with 6-week high-fat diet and 3-week exercise training interventions

first: Maria

last: Vamvini

first: Pasquale

last: Nigro

first: Laurie

last: Goodyear

first: Manolis

last: Kellis


title: Dissection of obesity-exercise axis in adipose-muscle tissues

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

overall_design: Refer to individual Series


title: Cholangiocarcinoma cell line (CCA cell line KKU-213A) treated in lactic acidosis condition

city: Kumamoto

first: Ubonrat

last: Thamrongwaranggoon

address: 2-2-1 Honjo,Chuo-ku,

department: Medical Cell Biology

country: Japan

institute: Institute of Molecular Embryology and Genetics

summary: To understand the effect of lactic acidosis in cholangiocarcinoma cell line. Cells were cultured in different conditions: lactic acidosis, lactosis, acidosis and control. We found that lactic acidosis promoted aggressiveness of cancer cells and reprograming of metabolic.

first: Shinjiro

last: Hino

first: Mitsuyoshi

last: Nakao


title: Impact of circadian rhythm in obtaining reference profiles of exRNAs in healthy individuals (2)

first: Ionita

middle: Calin

last: Ghiran

state: MA

address: 3 Blackfan Circle

department: Medicine

institute: Beth Israel Deaconess Medical Center

type: Non-coding RNA profiling by high throughput sequencing

summary: Blood was collected from healthy individuals in the morning, afternoon and evening, and plasma analyzed by RNA-seq. Plasma from two donors were not included due to excessive hemolysis in samples from two data points. One datapoint -afternoon- from donor 3 was also not included due to excessive hemolysis.

overall_design: 17 samples from 6 subjects, 3 time points (8:30am, 2:30pm, 6:30pm) from each subject.


title: The histone H3K36 demethylase Fbxl11 plays pivotal roles in the development of retinal late-born cell types [RNA-seq]

city: Tokyo

first: Toshiro

last: Iwagawa

address: Hongo 7-3-1, Bunkyo-ku

institute: The University of Tokyo

summary: Histone methylation plays a vital role in retinal development. However, the role of histone H3K36 methylation in retinal development is not clear. We examined the role of H3K36 methylation by loss-of-function analysis of H3K36me1/2 demethylases.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for Fbxl11-CKO retina and its WT control at postnatal day 7.

first: Masaya

last: Fukushima

first: Sumiko

last: Watanabe


title: Genetic and epigenetic profiling identifies two distinct classes of spinal meningiomas

city: Hamburg

first: Krystian

middle: Daniel

last: Fita

address: Martinistrasse 52

department: Department of Neurosurgery

institute: University Medical Center Hamburg-Eppendorf

summary: Spinal meningiomas account for 1.2-12% of all meningiomas and 25-45% of all spinal tumours. About 20% of intracranial, but also 4.6% of spinal meningiomas recur and require additional treatment. The classification of intracranial meningiomas has evolved considerably in recent years and uses genetic [1,2,4] as well as epigenetic parameters [3,5] in order to more precisely predict the patients’ prognosis and to lay the ground for therapeutic regiments that are adapted to the aggressiveness of a patient’s tumor. On the other hand, spinal meningiomas are missing in many of the large cohorts that were gathered for the molecular profiling of meningiomas. Also, they have never been thoroughly analyzed separately, and their classification still relies on histopathological findings solely.  We analysed 65 tumour samples from 63 patients, who had histologically proven spinal meningioma to perform genetic and epigenetic profiling. Clinical features are described in Supplementary Table 1, online resource. T-distributed Stochastic Neighbor Embedding (t-SNE) analysis of genome-wide DNA methylation data shows that most spinal meningiomas separate from cranial meningiomas (Fig. 1A&B) and form two distinct clusters.

overall_design: 65 tumor samples of spinal meningiomas from 63 patients with histologically confirmed spinal meningioma. 3 samples from recurrent spinal meningiomas.

first: Franz

middle: L

last: Ricklefs

middle: D

first: Malte

last: Mohme

first: Christian

last: Mawrin

first: Ramin

last: Rahmanzade

first: Felix

last: Sahm

first: Lasse

last: Dührsen

first: Carolin

last: Göbel

first: Katrin

last: Lamszus

first: Manfred

last: Westphal

first: Ulrich

last: Schüller

first: Sven

middle: O

last: Eicker


title: The histone H3K36 demethylase Fbxl11 plays pivotal roles in the development of retinal late-born cell types [Cut&Tag]

overall_design: Cleavage Under Targets and Tagmentation (CUT&Tag) for the histone modifications H3K36me2 and H3K36me3 in Fbxl11-CKO or control WT retinas at postnatal day 1.


title: Autophagy inhibition impairs leukemia stem cell function in FLT3-ITD AML but has antagonistic interactions with tyrosine kinase inhibition

city: Birmingham

first: Ravi

last: Bhatia

address: 2555A North Pavilion, 1802 6th Avenue South

department: Division of hematology and oncology

institute: The university of Alabama at Birmingham

summary: The FLT3-ITD mutation is associated with poor prognosis in acute myeloid leukemia (AML). FLT3 tyrosine kinase inhibitors (TKIs) demonstrate clinical efficacy but fail to target leukemia stem cells (LSC) and do not generate sustained responses. Autophagy is an important cellular stress response contributing to hematopoietic stem cells (HSC) maintenance and promoting leukemia development. Here we investigated the role of autophagy in regulating FLT3-ITD AML stem cell function and response to TKI treatment. We show that autophagy inhibition reduced quiescence and depleted repopulating potential of FLT3-ITD AML LSC, associated with mitochondrial accumulation and increased oxidative phosphorylation. However, TKI treatment reduced mitochondrial respiration and unexpectedly antagonized the effects of autophagy inhibition on LSC attrition. We further show that TKI-mediated targeting of AML LSC and committed progenitors was p53-dependent, and that autophagy inhibition enhanced p53 activity and increased TKI-mediated targeting of AML progenitors, but decreased p53 activity in LSC and reduced TKI-mediated LSC inhibition. These results provide new insights into the role of autophagy in differentially regulating AML stem and progenitor cells, reveal unexpected antagonistic effects of combined oncogenic tyrosine kinase inhibition and autophagy inhibition in AML LSC, and suggest an alternative approach to target AML LSC quiescence and regenerative potential.

overall_design: Examination of Vehicle, Lys05, AC220 and Combniation in vivo effect by high throughput sequencing on LSK or GMP cells of transgenic FLT3-ITD mice

first: Shaowei

last: Qiu


title: The histone H3K36 demethylase Fbxl11 plays pivotal roles in the development of retinal late-born cell types.

first: Toshiro

last: Iwagawa


title: Single-cell transcriptome Atlas reveals protective characteristics of COVID-19 mRNA vaccine [scRNA-seq]

city: Shanghai

first: Xingguang

last: Liu

overall_design: Rhesus macaques received three doses of mRNA vaccine SW0123 or PBS. Then reesus macaque were challenged by SARS-CoV-2 2 weeks after the last vaccination. The lung tissues from rhesus amcaques were harvested and digested into single cell suspensions 1 week post SARS-CoV-2 infection.

first: Yong

last: Tan

first: Ang

last: Lin

first: Zhenzhen

last: Zhan


title: Astrocytic tau reduction prevents Ab-induced synaptotoxicity

city: Indianapolis

first: Cristian

last: Lasagna-Reeves

state: IN

address: 320 West 15th Street

department: Anatomy & Cell Biology

institute: Indiana University School of Medicine

summary: Differential gene expression analysis between WT and TauKO-derived astrocyte cultures

overall_design: Total mRNA purified from primary astrocyte cultures loaded on a nCounter Mouse Glial Profiling Panel. 770 genes analyzed. Downstream analyses and visualizations of gene expression datasets were performed using the NanoString nCounter Advanced Analysis Report software

first: Pablo

last: Cisternas

first: Xavier

last: Taylor

last: Martinez

first: Olando

last: Maldonado


title: Knocking out BATF improves CAR-T cell efficacy by resisting exhaustion and forming central memory cells

city: Beijing

first: Xingying

last: Zhang

address: No. 5, Yard 1, Beichen West Road, Chaoyang District

institute: Institute of Zoology, Chinese Academy of Sciences

summary: Chimeric antigen receptor modified T (CAR-T) cell therapy has limited efficacy against solid tumor, one major challenge is T cell exhaustion. To address this challenge, we performed a candidate gene screen using a hypofunction CAR-T cell model, and found that knocking out BATF improved the performance of CAR-T cells. In different types of CAR-T cells and mouse OT-1 cells, knocking out BATF endows T cells with improved resistance to exhaustion and better tumor eradication efficacy. We find that BATF binds to and up-regulates a subset of exhaustion genes in human CAR-T cells. Furthermore, BATF regulates the expression of genes involved in the development of effector and memory cells, and knocking out BATF shifts the population towards more central memory subset. Therefore, we conclude that BATF is a key factor limiting CAR-T cell function, and its depletion improves CAR-T cells efficacy against solid tumor.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design:
We established an in vitro CAR-T cell hypofunction model and identify that BATF drives exhaustion via binding to and upregulating related genes in CAR-T cells, as well as regulates CAR-T cell subtypes. Knocking out BATF improves CAR-T cells efficacy against solid tumor.

We sorted GFP-positive cells co-cultured with tumor at 0.1:1 E:T ratio at day 7, named as hypofunction M28Z. After being co-cultured with tumor cells for 24h at E: T=2:1 (achieved 90% tumor lysis), GFP-positive CAR-T cells were sorted and named as activated M28Z; CAR-T cells thawed from the cryopreserved stock were sorted as control (fresh M28Z). To further characterize these hypofunction CAR-T cells, we performed RNA-seq on CD8-positive cells isolated from these three groups mentioned above. In addition, to control for the influence of long-term cultivation on CAR-T cells, we sequenced CAR-T cells cultured alone for 7 days (named unstimulated M28Z). To investigate the role of BATF and IRF4 in CAR-T cell exhaustion, we performed RNA-seq analysis of M28Z, M28Z-BKO and IKO cells isolated from the hypofunction model. To further validate the function of BATF in human CAR-T cells, we over-expressed BATF in CAR-T cells (M28Z-BOE) by lentiviral transduction and RNA-seq was performed using M28Z, M28Z-BKO, M28Z-BOE after three rounds of tumor cell challenges. To further dissect the molecular mechanism, we performed ChIP sequencing (ChIP-seq) in M28Z CAR-T cells. To better dissect the role of Batf in primary T cells, RNA-seq was performed using OT-1 cells upon repetitive tumor challenge.

first: Haoyi

last: Wang

first: Miaomiao

last: Qiao

first: Chenze


title: Transcriptomic analysis of SH1000 under sigS over-expression

city: Tampa

first: Lindsey

last: Shaw

address: 4202 E. Fowler Ave.

department: CMMB

institute: University of South Florida

summary: Analysis of the transcriptome changes in vector control vs. sigS over-expression samples.

overall_design: S. aureus RNA was extracted to determine transcriptome changes upon the over expression of sigS.

first: Brooke

middle: R

last: Tomlinson

first: Amer

last: Ali

first: Karl

last: Thompson

middle: N


title: TET2 deficiency promotes MDS-associated leukemogenesis

city: Duarte

first: WEI

last: CHEN

state: CA

address: 1500 E Duarte Rd

institute: City of Hope National Medical Center

summary: Loss of function TET2 mutations are frequently seen in myelodysplastic syndrome (MDS) patients. Previous studies have demonstrated that TET2 deficiency enhances maintenance of MDS hematopoietic stem and progenitor cells (HSPCs). Nonetheless, the pathogenic role of TET2 in MDS progression remains elusive. Here, we demonstrate Tet2 knockout (KO) markedly accelerated malignant transformation in Nup98-HoxD13 (NHD13) transgenic mice and promotes leukemogenesis of HoxA9 transduction/transplant mice. Consistently, low TET2 level cooperating with high HOXA9 level predicts poor outcome of MDS patients. Notably, Tet2 KO conferred a clonal advantage to the HSPCs of NHD13 mice. Whole-exome sequencing revealed that Tet2 KO facilitates accumulation of mutations at genes associated with leukemogenesis, including Arih2, whose loss of function promotes MDS cells proliferation. Using 5-hydroxymethylcytosine immunoprecipitation coupled with high-throughput sequencing analysis, we found while Tet2 deletion decreased overall 5hmC levels, it also increased 5hmC distribution at certain mutation loci such as Arih2. Vitamin C treatment, which mimics Tet2/Tet3 restoration, blocked disease progression in Tet2-deficient NHD13 mice. Collectively, our findings demonstrate that TET2 activity governs occurrence of secondary mutations in MDS HSPCs, providing a rationale for enhancing TETs function to block MDS-malignant transformation.

overall_design: Bone marrow c-kit+ cells were selected from NHD13/Tet2-WT and NHD13/Tet2-KO mice, 5-hydroxymethylcytosine (5hmC) modified DNA fragments were further purified and immunoprecipited by anti-5hmC antibody for Next-Generation Sequencing

first: Ling

last: Li

first: Feiteng

last: Huang

first: Wei

last: Chen

first: Jinhui

first: Xiwei

last: Wu


title: RNA-seq for NB4 cell line in either the absence or presence of MZ1

city: Suzhou

first: Fang

last: Fang

state: Jiangsu

address: 92 Zhongnan street

institute: Children’s Hospital of Soochow University

summary: Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for NB4 cell line in either the absence or presence of MZ1

overall_design: 2 NB4 samples with no treatment and 2 NB4 samples with MZ1

first: Jian

last: Pan

first: Li

last: Ma


title: Single-cell transcriptome Atlas reveals protective characteristics of COVID-19 mRNA vaccine

first: Xingguang

last: Liu


title: Transcriptomic response to calcium in normal colon organoids is impacted by colon location and sex

city: Charlottesville

first: Matthew

last: Devall

address: 1335 Lee Street

institute: University of Virginia

summary: Here, we used bulk RNA-seq data derived from healthy colon organoids exposed to two differing calcium concentrations. Through the use of external single cell RNA-seq data, we estimate changes in cell composition and gene expression brought about by high calcium conditions and relate those effects to colorectal cancer.

overall_design: Analysis of the effects of carcinogen treatment on gene expression in colon organoids

first: Graham

last: Casey


title: Spatial transcriptomics reveal unnresolved wound repair as potential driver of PFA Ependymoma progression

city: NEW YORK

first: RUI

last: FU

address: 101 6th Ave

department: Computational Biology

institute: New York Genome Center

summary: Childhood brain tumor ependymoma remains incurable in approximately 50 percent of cases. No oncogenic mechanism has been firmly established for the commonest ependymoma variant posterior fossa subgroup A (PFA), impeding clinical advances. Uncovering how heterogeneous cell types within the tumor microenvironment interact is crucial to a complete understanding of PFA disease progression. The underlying cellular components of the PFA tumor microenvironment have been revealed by single cell transcriptomics, identifying divergent epithelial differentiation and EMT lineages. Here we utilize spatial transcriptomics (Visium) of 14 PFA samples to chart neoplastic and immune cell architecture and identify novel biological processes.

first: Rui

last: Fu

first: Greg

last: Norris

first: Nicholas

last: Willard

last: Foreman

first: Andrew

last: Donson


first: WEI

last: CHEN

overall_design: Three NHD13/Tet2fl/fl and five NHD13/Tet2fl/fl/Mx1-Cre mice from the same pair of breeders (NHD13/Tet2fl/fl and Tet2fl/fl/Mx1-Cre) were used . Tet2 was deleted by injection of poly(I:C) at 6-weeks-old and c-kit+ cells were isolated at 20-weeks-old. Genomic DNA was purified for Whole-Exome-Sequencing

first: L

first: F

first: W

first: M

first: J

last: Wang

first: X


title: TGFβ1 impairs the transcriptomic response to contraction in myotubes from women with polycystic ovary syndrome

city: Copenhagen

first: Ali

last: Altintas

address: Blegdamsvej 3B

department: NNF Center for Basic Metabolic Research

country: Denmark

institute: Copenhagen University

summary: Polycystic ovary syndrome (PCOS) is characterised by a hormonal imbalance affecting the reproductive and metabolic health of reproductive-aged women. Exercise is often recommended as a first-line therapy for women with PCOS to help improve their overall health however, women with PCOS are resistant to the metabolic benefits of exercise training. Here, we aimed to gain insight into the mechanisms responsible for such resistance to exercise in PCOS. We employed an in vitro approach with electrical pulse stimulation (EPS) of cultured skeletal muscle cells to explore whether muscle cells from women with PCOS have an altered gene expression signature in response to muscle contraction. Following EPS, 4,719 genes were differentially expressed (FDR < 0.05) in myotubes from women with PCOS compared to only 173 in healthy control women. Both groups included genes involved in skeletal muscle contraction. We also determined the effect of two transforming growth factor-beta ligands that are elevated in plasma of women with PCOS, the transforming growth factor beta-1 (TGFβ1) and the anti-müllerian hormone (AMH), alone and on the EPS-induced response. While AMH (30 ng/ml) had no effect, TGFβ1 (5 ng/ml) induced the expression of extracellular matrix genes and impaired the exercise-like gene expression signature in myotubes from women with and without PCOS in response to EPS by interfering with key processes related to muscle contraction, calcium transport and actin filament. Collectively, our findings suggest that while the fundamental gene expression responses of skeletal muscle to contraction is intact in PCOS, elevated circulating factors like TGFβ1 may be responsible for the impaired adaptation to exercise intervention in women with PCOS.

overall_design: Primary myotube cultures were established from skeletal muscle biopsies (vastus lateralis) obtained from six overweight insulin resistant PCOS women (PCOS) and six healthy lean control women (CTRL), all aged between 18-40 years old. Myotubes were treated with TGFB1 (5ng/ml) or AMH (30ng/ml), and also with and without EPS (11.5 V, 2 ms, 1Hz). RNA-seq analysis was performed with primary myotubes from five women with PCOS and five healthy women (an additional myotube sample for the healthy women was included for the non-treated condition only).

first: Luke

middle: C

last: McIlvenna

last: Altıntaş

first: Rhiannon

last: Patten

middle: J

last: McAinch

first: Raymond

last: Rodgers

first: Nigel

last: Stepto

first: Romain

last: Barrès

first: Alba

last: Moreno-Asso


title: Transcriptomic profiling of sporadic Alzheimer’s disease patients

city: La Jolla

first: Shankar

last: Subramaniam

address: 9500 Gilman Drive

department: Department of Bioengineering

institute: University of California, San Diego

summary: Alzheimer’s disease (AD) manifested before age 65 is commonly referred to as early-onset AD (EOAD). While the majority (> 90%) of EOAD cases are not caused by autosomal-dominant mutations in PSEN1, PSEN2, and APP, they do have a higher heritability (92–100%) than sporadic late-onset AD (LOAD, 70%). Although the endpoint clinicopathological changes, i.e., Aβ plaques, tau tangles, and cognitive decline, are common across EOAD and LOAD, the disease progression is highly heterogeneous. This heterogeneity, leading to temporally distinct age at onset (AAO) and stages of cognitive decline, may be caused by myriad combinations of distinct disease-associated molecular mechanisms. We and others have used transcriptome profiling in AD patient-derived neuron models of autosomal-dominant EOAD and sporadic LOAD to identify disease endotypes. Further, analyses of large postmortem brain cohorts demonstrate that only one-third of AD patients show hallmark disease endotypes like increased inflammation and decreased synaptic signaling. Areas of the brain less affected by AD pathology at early disease stages—such as the primary visual cortex—exhibit similar transcriptomic dysregulation as those regions traditionally affected and, therefore, may offer a view into the molecular mechanisms of AD without the associated inflammatory changes and gliosis induced by pathology. To this end, we analyzed AD patient samples from the primary visual cortex (19 EOAD, 20 LOAD) using transcriptomic signatures to identify patient clusters and disease endotypes. Interestingly, although the clusters showed distinct combinations and severity of endotypes, each patient cluster contained both EOAD and LOAD cases, suggesting that AAO may not directly correlate with the identity and severity of AD endotypes.

overall_design: Alzheimer’s disease (AD) and healthy, non-demented control (NDC) samples were obtained from brain bank of samples preserved at the UC San Diego Shiley-Marcos Alzheimer’s Disease Research Center (UCSD ADRC), extracting tissue from the occipital lobe (primary visual cortex, Brodmann Area 17, Bm-17) in accordance with UC San Diego IRB approval. A total of 48 samples were selected: 8 NDC and 40 AD patient samples. The 40 AD samples were selected based on their lack of alternative diagnosis (e.g. Lewy Body Dementia, hippocampal sclerosis) and stratified into two groups based on the age of onset of AD: early-onset, i.e. those with an age of onset less than 60 years (n=19), and late-onset, i.e. those with an age of onset between 70 and 80 years (n=21)

middle: B

last: Caldwell

first: Balaji

last: Anantharaman

first: Srinivasan

last: Ramachandran

first: Douglas

last: Galasko

first: Paula

last: Desplats

first: Steven

last: Wagner


title: Subinhibitory Concentrations of Antibiotics Alter the Response of Klebsiella pneumoniae to Components of Innate Host Defense

city: Hamilton

first: Dan

last: Sturdevant

state: MT

address: 903 S 4th street

department: NIAID

institute: NIH

summary: Carbapenem-resistant Klebsiella pneumoniae classified as multilocus sequence type 258 (ST258)are a problem in healthcare settings in many countries globally. ST258 isolates are resistant tomultiple classes of antibiotics and can cause life-threatening infections, such as pneumonia andsepsis, in susceptible individuals. Treatment strategies for such infections are limited. Hence,understanding the response of K. pneumoniae to host factors in the presence of antibiotics couldreveal mechanisms employed by the pathogen to evade killing in the susceptible host, as well asinform treatment of infections. Here, we investigated the ability of subinhibitory concentrationsof antibiotics to alter K. pneumoniae capsule polysaccharide (CPS) production and survival innormal human serum. Several antibiotics tested enhanced ST258 survival in normal humanserum. Unexpectedly, subinhibitory concentrations of mupirocin increased survival in 7 of 10clinical isolates tested, and caused up-regulated expression of CPS biosynthesis genes and CPSproduction in a selected ST258 clinical isolate (34446) compared with untreated controls.Additionally, mupirocin treatment caused a reduction in the deposition of the serum complementproteins C3b and C5b-9 on the surface of ST258. Transcriptome analyses with isolate 34446indicated that genes implicated in serum resistance, such as aroE, csrD, pyrB, pyrC and traT,were up-regulated following mupirocin treatment. In conclusion, mupirocin causes changes inthe K. pneumoniae transcriptome that likely contribute to the observed decrease in serumsusceptibility via a multifactorial process. Whether these responses are triggered by othercomponents of host defense or therapeutics that were not tested here merits further investigation.

overall_design: treatment conditions compared of Klebsiella pneumoniae

first: Clement

last: Opoku-Temeng

first: Brett

last: Freedman

first: Scott

last: Kobayashi

first: Liang

last: Chen

first: Barry

last: Kreiswirth

first: Frank

last: DeLeo


title: Genome-wide screen reveals UL49 is an essential vPIC subunit that transcribes late Human Cytomegalovirus genes

city: Clayton

first: Monash

middle: Bioinformatics

last: Platform

state: VIC

address: Wellington Road

country: Australia

institute: Monash Bioinformatics Platform

summary: More than half the world's population is infected with Human Cytomegalovirus (HCMV), increasing risks for the immuno-compromised, and causing significant congenital birth defects. The HCMV genome encodes >170 proteins; many that remain uncharacterised, which restricts development opportunities for new antivirals. In this study, a molecular assay was developed to conduct a genome-wide HCMV screen to identify genes that function during late stages of infection. Saliently, loss of UL49 completely abolished production of infectious virions. During infection, UL49 displayed leaky late expression kinetics and nuclear localization. Functionally, UL49 is as an essential subunit of the viral pre-initiation complex (vPIC), enhancing transcription of late viral genes containing non-canonical TATT motif promoters. RNA-seq revealed the full repertoire of vPIC-regulated genes, including transcripts coding for capsid subunits, envelope glycoproteins and egress-associated tegument proteins. Therefore, UL49 together with other vPIC subunits, serve as fundamental HCMV effectors that govern successful completion of the replication cycle.

sample_organism:
Homo sapiens
Human betaherpesvirus 5

platform_organism:
Homo sapiens
Human betaherpesvirus 5

overall_design: Comparative gene expression profiling analysis of RNA-seq data for HCMV AD169 WT and vPIC subunit KO infected MRC5 fibroblasts at 72 HPI.

first: Declan

last: Turner

first: Adele

last: Barugahare

first: Brendan

middle: E

last: Russ

first: Stephen

first: Rommel

last: Mathias


title: Favine/CCDC3 deficiency accelerated atherosclerosis and thrombus formation is associated with decreased MEF2C-KLF2 pathway

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary:
Currently, no mouse models manifest calcification and thrombus formation, which is frequently associated with human atherosclerosis. We demonstrated that lack of Favine/CCDC3 in apoE knockout mice accelerated atherosclerosis accompanied by large cholesterol crystals and calcification, and also promoted thrombus formation in the left ventricle and arteries. Circulating Favine was detectable in WT mouse lasma. RNA-sequencing analysis of aortae in DKO mice showed similar gene expression patterns of human atherosclerosis with unstable and vulnerable plaques. Importantly, human FAVINE mRNA expressions were lower in atheroma plaque than in adjacent intact aortic tissue and decreased with the progression of atherosclerosis. Pathway analysis of aortae in DKO mice suggested the decrease of the MEF2C-KLF2-mediated transcriptional pathway. Favine insufficiency and its attenuated downstream pathways may increase atherosclerosis progression with calcification and thrombus, which have not previously been fully modeled in experimental animals. Favine and its downstream pathways may have
therapeutic potential for atherosclerosis.

overall_design: To investigate the mechanisms of progression of atherosclerosis, calcification, and thrombosis in DKO mice, bulk RNA-seq analysis of the aortas of ApoE KO mice and DKO was carried out.

first: Sachiko

first: Shunbun

last: Kita