Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide screen of CREB and CRTC2 occupancy in LKB1 mutant NSCLC cell line A549

ABSTRACT: Genome wide screen of CREB and CRTC2 occupancy in LKB1 mutant NSCLC cell line A549

PROVIDER: PRJNA529194 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Genome wide screen of CREB and CRTC2 occupancy in LKB1 mutant NSCLC cell line A549

Project description:CREB and CRTC2 ChIPseq analysis in LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

2019-07-26 | GSE128871 | GEO

RNA-seq profiling of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:Investigating transcriptional profile of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β

2023-05-11 | GSE214823 | GEO

LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

Project description:LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

| PRJNA529192 | ENA

Genome wide screen of H3K27ac enrichment in WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:H3K27ac ChIP-seq analysis in WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β

2023-05-11 | GSE214822 | GEO

Gene responses to LKB1 overexpression in NSCLC cell line A549

Project description:Differential gene expression analysis of LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

2019-07-05 | GSE128872 | GEO

CREB Coactivators CRTC2 and CRTC3 Modulate Bone Marrow Hematopoiesis

Project description:Populations of circulating immune cells are maintained in equilibrium through signals that enhance the retention or egress of hematopoietic stem cells (HSCs) from bone marrow (BM). Prostaglandin E2 (PGE2) stimulates HSC renewal and engraftment, for example, via induction of the cAMP pathway. Triggering of PGE2 receptors increases HSC survival in part via the PKA-mediated induction of the CREB signaling pathway. PKA stimulates cellular gene expression by phosphorylating CREB at Ser133 and by promoting the dephosphorylation of the cAMP Responsive Transcriptional Coactivators (CRTCs). We show here that disruption of both CRTC2 and CRTC3 causes embryonic lethality, and that a single allele of either CRTC2 or CRTC3 is sufficient for viability. CRTC2 knockout mice that express one CRTC3 allele (CRTC2/3m mice) develop neutrophilia and splenomegaly in adulthood due to the up-regulation of Granulocyte-Colony Stimulating Factor (G-CSF); these effects are reversed following administration of neutralizing anti-G-CSF antiserum. Adoptive transfer of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype on WT recipients. Indeed, targeted disruption of both CRTC2 and CRTC3 in stromal cells with a mesenchymal Prx1-Cre transgene also promoted this phenotype. Depletion of CRTC2/3 was found to decrease the expression of Suppressor of Cytokine Signaling 3 (SOCS3), leading to increases in STAT3 phosphorylation and to the induction of CEBPb, a key regulator of the G-CSF gene. As small molecule inhibition of JAK activity disrupted CEBPb induction and reduced G-CSF expression in CRTC2/3m stromal cells, our results demonstrate how cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to BM homeostasis.

2018-02-01 | GSE103999 | GEO

CREB Coactivators CRTC2 and CRTC3 Modulate Bone Marrow Hematopoiesis

Project description:CREB Coactivators CRTC2 and CRTC3 Modulate Bone Marrow Hematopoiesis

| PRJNA407926 | ENA

Gene responses to LKB1 overexpression in NSCLC cell line A549

Project description:Gene responses to LKB1 overexpression in NSCLC cell line A549

| PRJNA529196 | ENA

CREB regulated transcriptional coactivator 2 proteome landscape is plausibly modulated by SREBF1

Project description:CRTC2 is a critical transcription cofactor that induces the glucose homeostatic genes by activating CREB. However, energy homeostasis is maintained by multiple pathways, therefore, it is possible that CRTC2 may interact with other transcription factors, especially under metabolic stress. Thereby, CRTC2 liver-specific knockout mice were created and the global proteome, phosphoproteome and acetylome from liver tissue under the high fat diet conditions were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and bioinformatics analysis. As expected, differentially expressed proteins (DEPs) are enriched in metabolic pathways that were subsequently corroborated by animal experiments. The consensus DEPs from these datasets were used as seed proteins to generate a protein-protein interaction (PPI) network using STRING and GeneMANIA identified fatty acid synthase (FASN) as the mutually relevant protein. Additional local-PPI (LPPI) analysis of CRTC2 and FASN with DEPs, SREBF1 was found to be a common mediator. CRTC2/CREB and SREBF1 are transcription factors, DNA-binding motif analysis showed multiple CRTC2/CREB regulated genes also possess SREBF1 binding motifs that unveil the possible induction by CRTC2/SREBF1 complex, which is reinforced by structural analysis. Thus, CRTC2/SREBF1 complex plausibly modulate the transcription of multiple proteins that fine-tune the cellular metabolism under metabolic stress.

2023-10-24 | PXD039817 | Pride

AXL targeting restores PD-1 blockade sensitivity of STK11/LKB1 mutant NSCLC through expansion of TCF1+ CD8 T cells

Project description:Mutations in STK11/LKB1 in non-small cell lung cancer (NSCLC) are associated with poor patient responses to immune checkpoint blockade (ICB) and introduction of a Stk11/Lkb1 (L) mutation into murine lung adenocarcinomas driven by mutant Kras and Trp53 loss (KP) resulted in an ICB refractory syngeneic KPL tumor. Mechanistically this occurred because KPL mutant NSCLCs lacked TCF1-expressing CD8 T cells, a phenotype recapitulated in human STK11/LKB1 mutant NSCLCs. Systemic inhibition of Axl results in increased type I interferon secretion from dendritic cells that expanded tumor-associated TCF1+ PD-1+ CD8 T cells, restoring therapeutic response to PD-1 ICB for KPL tumors. This was observed in syngeneic immunocompetent mouse models and in humanized mice bearing STK11/LKB1 mutant NSCLC human tumor xenografts. NSCLC patients with identified STK11/LKB1 mutations receiving bemcentinib and pembrolizumab demonstrated objective clinical response to combination therapy. We conclude that AXL is a critical targetable driver of immune suppression in STK11/LKB1 mutant NSCLC.

2022-01-24 | GSE194166 | 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