Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A TNFR2-hnRNPK axis promotes primary liver cancer development via activation of YAP signaling in hepatic progenitor cells

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, Tnfrsf1α-/- and Tnfrsf1β-/- (with or without TNFα treat) HPCs Transcriptomes.The mRNA profiles of Wild Type, Tnfrsf1α-/- and Tnfrsf1β-/- (with or without TNFα treat) HPCs were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level . qRT–PCR validation was performed using TaqMan and SYBR Green assays.We performed RNA-seq analysis to assess the global impacts of TNFR2 on HPCs' response to TNFα. Upon TNFα treatment, 519 genes were significantly upregulated in wild type HPCs . 39% of these genes (203 out of 519) were further upregulated in Tnfrsf1a-/- HPCs treated with TNFα. However, these 203 genes were dramatically downregulated in TNFα-treated Tnfrsf1b-/- HPCs relative to their expression in either TNFα-treated Tnfrsf1a-/- HPCs or wild type HPCs, indicating an inhibitory role for deletion of TNFR2 in the regulation of these genes.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE166627 | GEO | 2021/06/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TNFα/TNFR2 axis mediates natural killer cell proliferation by enhancing their glycolytic plasticity

Project description:Natural Killer (NK) cells are predominant innate lymphocytes that provide the early response during infection. NK cells undergo metabolic switch to fuel augmented proliferation and activation following infection. TNFα is a well-known inammatory cytokine that enhances NK cell function, however, a mechanism for stimulation is not well established. Here, we demonstrated that upon infection/inammation, NK cells upregulate the expression of TNF receptor 2 (TNFR2), which is associated with increased proliferation, metabolic activity and effector function. Notably, IL-18 can induce TNFR2 on NK cells, augmenting their sensitivity towards TNFα. Mechanistically, TNFα-TNFR2 signaling induces CD25 (IL-2Rα) expression on NK cells predominantly by autocrine mode, leading to a metabolic switch towards aerobic glycolysis. Accordingly, genetic ablation of TNFR2 curtails the CD25 upregulation and TNFα-induced glycolysis, leading to impaired NK cell proliferation during MCMV infection in vivo. Collectively, our results delineate the crucial role of the TNFα-TNFR2 axis in NK cells for proliferation, glycolysis, and effector function via CD25 induction.

2023-09-26 | GSE235545 | GEO

cFLIP prevents TNFR1-dependent lethal dermatitis and TNFR1-independent blockade of epidermal differentiation

Project description:Cellular FLICE-inhibitory protein (cFLIP) prevents the development of dermatitis by blocking TNFα-dependent apoptosis of keratinocytes. However, it is unclear whether TNFα-independent signal might also contribute to the development of dermatitis in epidermis-specific Cflar-deficient (Cflar) mice. Here we show that Cflar;Tnfrsf1a-/- mice were born at the expected Mendelian ratio, but developed severe dermatitis and succumbed soon after birth. While keratinocytes still died by apoptosis, expression of epidermal differentiation markers, such as Loricrin, Filaggrin, and Keratin (Krt)10, but not Krt5 were severely downregulated in the skin of Cflar;Tnfrsf1a-/- mice at both mRNA and protein levels. Conversely, inflammatory cytokines, such as interleukin (IL)-6 and Il17a were elevated in the skin of Cflar ;Tnfrsf1a-/- mice. Treatment of primary keratinocytes with IL-6, to a lesser extent IL-17A suppressed expression of Loricrin, Filaggrin, and Krt10. Together, cFLIP suppresses TNFR1-independent apoptosis of keratinocytes and prevents IL-6-dependent blockade of epidermal differentiation.

2020-04-01 | GSE99379 | GEO

Analysis of expression changes between IL-33 Knock out and WT mice in skin chronic inflammation

Project description:To find differential expression gene between IL-33KO and WT mice, we collected skin epithelial RNA sample after all of mice were treated with DNFB for 22 days. (allergen treat) After RNA-seq analysis, we got 203 genes which showed different expression level between IL-33KO and WT mice after allergen treated.

2021-01-28 | GSE149578 | GEO

Expression data of mRNA from wild-type A549 cells and microRNA-203 knockout A549 cells during H5N1 infections

Project description:MicroRNA-203 was up-regulated markedly upon H5N1 virus infection. To identify the potential target genes of miR-203, we constructed a miR-203 knockout A549 cell line. Then wild-type and miR-203 knockout A549 cells were mock-infected or infected with H5N1 virus for 48h. The Agilent Whole Human Genome Oligo Microarray was performed to analyze the mRNA expression profiling. Meanwhile, the online tool TargetScanHuman (http://www.targetscan.org/vert_71/) was used to predict biological targets of miR-203. We combined the predicted genes with the genes differentially expressed in wild-type and miR-203 knockout A549 cells, and preliminarily identified some candidate mRNAs. Then more experiments were performed to further verify these target genes, such as dual-luciferase reporter assay, quantitative real-time PCR or Western blot analysis.

2018-05-09 | GSE107089 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [YX-FLI1_EM]

Project description:Background: Familial platelet disorder (FPD) is an autosomal dominant disease caused by a heterozygous germline mutation inRUNX1. FPD patients show not only thrombocytopenia with platelet dysfunction, but also a high level of developing hematological malignancies, strongly suggesting that FPD is in a precancerous state. However, the DNA methylation status of FPD has not yet been elucidated due to no animal models for FPD and the difficulty in obtaining FPD patient-derived samples. Results: We found that differentiation efficiencies into HPCs and megakaryocytes was reduced in the FPD-mimicking cells, which were established by genome editing for human iPS cells as a FPD-model, compared with those of wild-type cells. The FPD-mimicking HPCs were subjected to DNA methylation analysis, and the HPCs showed the distinct DNA methylation patterns compared to wild-type HPCs. Furthermore, we demonstrated a putative causative transcription factor of the differential DNA hypermethylation, which are involved in both promoting the binding site-directed DNA demethylation and regulating megakaryopoiesis.

2024-02-26 | GSE249049 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [WES]

2024-02-26 | GSE245770 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [FLI1_EM]

2024-02-26 | GSE245769 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [EM]

2024-02-26 | GSE245765 | GEO

Control, TNFα and TNFα+JNK I treated GSCs

Project description:Control, TNFα and TNFα+JNK I treated GSCs

| PRJNA799754 | ENA

Quantitative Analysis of Wild Type and miR-203 KO transcriptomes in the rat endometrial adenocarcinoma cell line RUCA-I

Project description:Purpose: identification of mRNAs that are potential targets of miR-203 in the endometrium and endometrial carcinoma Methods: mRNA profiles of three batches of wild-type (WT) and three independently generated miR-203 knockout (miR-203 KO) RUCA-I cells were produced by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped between 30 and 50 million sequence reads per sample to the rat genome (build rn6) and identified 26751 transcripts of which 1591 are differentially expressed in WT and miR-203 KO cells (p<0.05).

2017-03-10 | GSE95850 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data