Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis after selective expression of coagulation factor FVII

ABSTRACT: Gene expression analysis after selective expression of coagulation factor FVII

PROVIDER: PRJNA491486 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression analysis after selective expression of coagulation factor FVII

Project description:Analysis of coagulation factor FVII-induced breast cancer cell transformation at gene expression level. The hypothesis tested in the present study was that expression of FVII upregulates genes involved in epithelial-to-mesenchymal transition and transformation. Results provide important information on the cellular response to tumor FVII expression with respect to pro-oncogenic programs .

2018-09-18 | GSE120047 | GEO

Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression

Project description:Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression

| PRJNA429757 | ENA

Expression of the MET oncogene correlates with upregulation of coagulation factor XII and procoagulant disorders in colorectal cancer

Project description:Cancer patients often develop hemostasis disorders whose pathogenesis is poorly understood. Previous work in mouse models has shown that these disorders can be sustained by the MET oncogene by transcriptional upregulation of hemostasis genes. Here we investigated the correlation between the procoagulant state of colorectal cancer patients, and overexpression of MET and hemostasis genes in the tumor. We found that, in a patient subset, blood levels of D-dimer and coagulation factor XII (F12) were frequently elevated, and reverted towards normality after surgery. Global expression profiling of tumor tissues and adjacent mucosae revealed a significant correlation between high D-dimer levels in the blood, and overexpression of MET in the tumor. An “hemostasis gene signature”, including F12, cyclo-oxygenase 2, thromboxane synthase-1, plasminogen activator inhibitor-1, urokinase-type plasminogen activator and protein C receptor was associated with MET overexpression. This association was confirmed in an independent 173-sample CRC dataset. The mechanistic link between MET signaling and F12 expression was established experimentally in cell lines. These data indicate that MET contributes to the pathogenesis of coagulation disorders in CRC by upregulation of hemostasis genes including F12, and provide a candidate biomarker for the CRC-associated procoagulant state.

2022-12-30 | GSE52060 | GEO

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

Project description:MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.

2020-07-15 | ST001429 | MetabolomicsWorkbench

Gene expression analysis after selective expression of tissue factor isoforms

Project description:Analysis of TF isoform-induced breast cancer cell transformation at gene expression level. The hypothesis tested in the present study was that expression of TF isoforms upregulate genes involved in proliferation and transformation, while downregulating genes involved in cell cycle arrest and apoptosis. Results provide important information on the cellular response to TF expression with respect to pro-oncogenic programs . Total RNA obtained from an MCF-7-based cell model (2A3-3) expressing full length tissue factor (2A3-3-flTF) or alternatvively spliced tissue factor (2A3-3-asTF) compared to cells expressing an empty vector control (2A3-3-pcDNA).

2012-10-27 | E-GEOD-41872 | biostudies-arrayexpress

Gene expression analysis after selective expression of tissue factor isoforms

Project description: Not available

| S-ECPF-GEOD-41872 | biostudies-other

microRNA profile of control vehicle- and coagulation protease factor VIIa-released endothelial extracellular vesicles

Project description:microRNA profile of control vehicle- and coagulation protease factor VIIa-released endothelial extracellular vesicles

| PRJNA758366 | ENA

microRNA profile of control vehicle- and coagulation protease factor VIIa-released endothelial extracellular vesicles

Project description:Coagulation protease factor VIIa (FVIIa) is shown to induce anti-inflammatory and barrier protective effects via endothelial cell protein C receptor (EPCR)-dependent, protease-activated receptor-1 (PAR1)-mediated cell signaling. FVII-EPCR-PAR1 signaling also induces the release of extracellular vesicles from endothelial cells. To obtain clues on whether microRNA (miR) carried out by FVIIa-released EEVs contribute to anti-inflammatory and barrier protective effects, we analyzed miR expression in control- and FVIIa-released EEVs by deep sequencing. These data revealed that several anti-inflammatory miR expression was higher (more than 2-fold) in FVIIa-released EEVs compared to control EEVs, the most predominant being miR10a-5p. The differential expression of miR10a-5p and several other abundant miRs were validated by qRT-PCR. Subsequent in vitro and in vivo experiments showed that miR10a in FVIIa-released EEVs contribute to anti-inflammatory and barrier protective effects.

2021-08-29 | GSE182925 | GEO

Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development

Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) areis a major cause for acquired thrombophilia. Here we test the effect of specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) on the activation of monocytes by aPL. NGS data show that aPL-induced proinflammatory and prothrombotic activation of monocytes, but not interferon regulated gene induction is prevent by NAPc2.

2024-03-21 | GSE252972 | GEO

Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.

Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) are a major cause for acquired thrombophilia. Here we show that specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) prevents the the development of persistent aPL and circulating phospholipid-reactive B1 cells in latent viral infection and lupus prone MRL-lpr mice. NGS mRNA profiling of splenic DC in lupus mice treated with NAPc2 versus saline control uncovered a suppression of dendritic cell activation in the spleen.

2024-03-21 | GSE252397 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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