Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell sequecing of LCMV-specific WT and HIF-1a-deficient CD8 T cells isolated from LCMV-Clone13 infected host mice

ABSTRACT: Single-cell sequecing of LCMV-specific WT and HIF-1a-deficient CD8 T cells isolated from LCMV-Clone13 infected host mice

PROVIDER: PRJNA882768 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Single-cell sequecing of LCMV-specific WT and HIF-1a-deficient CD8 T cells isolated from LCMV-Clone13 infected host mice

Project description:To determine the role of hypoxia-inducible factor 1 alpha (HIF-1a) in exhausted T cells, we crossed Hif1a-fl/fl Cd4-Cre mice to tdTomato+ P14 animals and adoptively co-transferred equal numbers of WT and HIF-1a-deficient P14 CD8+ T cells into chronically infected WT host mice. 21 days post infection, we retrieved GFP+ (WT) and tdTomato+ (HIF-1a-deficient) donor P14 T cells by FACS sorting and subjected CITE-seq antibody-barcoded WT and HIF-1a-deficient CD8+ P14 T cells to multiplexed scRNA sequencing analysis.

2023-09-22 | GSE213847 | GEO

Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma

2012-02-25 | GSE27523 | GEO

Citrullination modulation maintains HIF-1A stabilization to drive tumor progression

Project description:HIF-1 (Hypoxia-inducible factor 1) is the master regulator responding to hypoxic conditions. Here, we found that HIF-1A is citrullinated by peptidyl arginine deiminase 4 (PADI4) at arginine 698, promoting HIF-1A stabilization and thus HIF-1-driven tumor growth. The knockdown of PADI4 could dramatically decrease HIF-1 protein expression without affecting the mRNA level, and this could be rescued by the proteasome inhibitor MG132 treatment under hypoxia. And PADI4-HIF-1A interaction is critical for HIF-1A stability and tumor progression, depending on the enzymatic activity of PADI4 and the pocket structure of PADI4. DHE, an FDA-approved agent for the treatment of migraine, was found serve as a potential antitumor agent throgh disrupting PADI4-HIF-1A interaction and suppressing HIF-1A stability. Taken together, we found the anti-tumor effect of DHE due to its effect on blocking PADI4-HIF-1A interaction and downregulating HIF-1A pathway in cancer cells. To figure out the influence of DHE on liver cancer cell under hypoxia, we treated Hep3B cell lines with two does DHE in 6 hours under Hypoxia and extracted mRNA for furthur RNA seq.

2024-05-28 | GSE233772 | GEO

Defective mitochondrial cardiolipin remodeling dampens HIF-1a expression in hypoxia

Project description:Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin-remodeling, upon loss of the cardiolipin acyl transferase Tafazzin, mutes HIF-1a signaling in hypoxia. Tafazzin-deficiency does not affect posttranslational HIF-1a regulation but rather HIF-1a gene-expression, a dysfunction recapitulated in iPSCs-derived cardiomyocytes from Barth Syndrome patients with Tafazzin-deficiency. RNAseq analyses confirmed drastically altered signaling in Tafazzin mutant cells. In hypoxia, Tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-kB activation and concomitantly HIF-1a gene-expression. In agreement, Tafazzin-deficient mice hearts display reduced HIF-1a levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondrial cardiolipin-remodeling dampens HIF-1a signaling through inactivation of a non-canonical signaling pathway: Lack of NF-kB activation through reduced mitochondrial ROS production diminishes HIF-1a transcription.

2018-09-12 | GSE119775 | GEO

Expression data from Mesenchymal progenitor cells knocked down for HIF-1a or HIF-2a expression

Project description:HIF-1a and HIF-2a are expressed at high levels in mesenchymal progenitors compared to more committed mesenchymal cells and hematopoietic cells. HIF-factors could therefore have a role in the regulation the biology of mesenchymal progenitors and their functions, like the non cell-autonomous maintenance of hematopoietic progenitors. We used microarrays to detail the global program of gene expression regulated by HIF-1a or HIF-2a in mesenchymal progenitors Mesenchymal progenitors were FACS-sorted and cultured in low oxygen concentration for few days. Once cells started to form CFU-F colonies, we transduced them with shRNAs targeting specifically HIF-1a or HIF-2a. Four days after transduction, cells were collected and RNA extracted for microarray analysis.

2014-03-25 | E-GEOD-56141 | biostudies-arrayexpress

Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma

Project description:HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia. In this dataset, we identify specific HIF-1A and HIF-2A target genes in glioblastoma cells. 12 samples were analysed comprising 4 experimental conditions (normoxia scr, hypoxia scr, hypoxia siHIF1, hypoxia siHIF2) in triplicate. We made pairwise comparisons between the averages of each triplicate set to normoxia scr using the Partek suite.

2012-02-25 | E-GEOD-27523 | biostudies-arrayexpress

Expression data from Mesenchymal progenitor cells knocked down for HIF-1a or HIF-2a expression

2014-03-25 | GSE56141 | GEO

Expression profile after stable HIF-1a inhibition in gastric cancer cells under normoxic conditions

Project description:Based on the results of numerous clinical and preclinical analyses, the transcription factor HIF-1a has been identified as an important tumor-promoting factor and is considered to be an attractive target for cancer therapy. To further deconstruct the molecular nature of HIF-1a’s role in tumorigenesis, we have applied lentiviral shRNA transduction to establish HIF-1a-deficient gastric cancer cells. Interestingly, functional analyses failed to show a significant growth defect of HIF-1a-deficient gastric cancer cells in vitro and in vivo. These observations led us to propose that stable inactivation of HIF-1a resulted in efficient compensation enabling cell growth and, ultimately, tumor progression in a HIF-1a-independent manner. To better understand the mechanisms that control this compensation, we performed transcriptomics of control (“scrambled” (SCR)) and HIF-1a-deficient (HIF) gastric cancer cells. Analysis of hypoxia-inducible factor-1alpha (HIF-1a)-deficient gastric cancer cells under normoxia. The transcription factor HIF-1a is a key regulator of oxygen homeostasis and has been identified as an important tumor-promoting factor. Results provide insight into the role of HIF-1a in gastric carcinogenesis.

2017-02-11 | GSE57200 | GEO

ChIP-seq analysis of HIF-1a and HIF-2a binding in hypoxic cancer cell lines

Project description:Pan-genomic analysis of hypoxic HIF-1a and HIF-2a binding by ChIP-seq in cancer cell lines

2022-11-15 | GSE200203 | GEO

Global genomic profiling of HIF-1a-regulated genes in bone marrow B cells under hypoxia or normoxia

Project description:HIF-1a works as a stress-induced transcription factor to induce target genes mediating cell proliferation, meabolism and inflammation. To gain new insights into HIF-1a biology, we used high-throughput sequencing to analyze global HIF-1a transcriptional networks in WT or HIF-1a deficient bone marrow B cells under hypoxia or normoxia.

2022-02-24 | GSE163848 | 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