Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Unraveling the CDK9/PP2A/ERK network in transcriptional pause release and complement activation in KRAS-mutant cancers (MIA PaCa-2 )

ABSTRACT: Unraveling the CDK9/PP2A/ERK network in transcriptional pause release and complement activation in KRAS-mutant cancers (MIA PaCa-2 )

PROVIDER: PRJNA1128237 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Unraveling the CDK9/PP2A/ERK network in transcriptional pause release and complement activation in KRAS-mutant cancers (MIA PaCa-2 )

Project description:KRASG12C inhibitors (KRASG12Ci) AMG510 and MRTX849 have shown promising efficacy in clinical trials and been approved for the treatment of KRASG12C-mutant cancers. However, the emergence of therapy-related drug resistance limits their long-term potential. We measured gene expression using RNA-sequencing for pancreatic cancer cell line MIA PaCa-2 parental and their AMG510-resistant equivalent without treatment or treated with with G12C KRAS inhibitor AMG510.

2024-08-31 | GSE270796 | GEO

siRNA knockdown of C1GALT1 in MIA PaCa-2 cells

Project description:To determine the C1GALT1 regulated gene expression profile in MIA PaCa-2 cells.

2017-12-04 | GSE90668 | GEO

MIA PaCa-2 cells treated with Gemcitabine

Project description:Pancreatic cancer cells (MIA PaCa-2) were treated with Gemcitabine and overall protein changes were studied

2022-09-15 | PXD030861 | Pride

mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

Project description:mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

| PRJNA925906 | ENA

RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

Project description:RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

2022-05-01 | GSE169660 | GEO

mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

Project description:Pancreatic ductal adenocarcinoma, caused by activating mutation in K-Ras, is an aggressive malignancy due to its early invasion and matastasis. Ral GTPases, negatively regulated by RalGAP, are activated downstream of Ras and play a crucial role in development and progression of pancreatic ductal adenocarcinoma. However, the underlying mechanisms remain unclear. We used microarrays to detail the global programme of gene expression underlying the human pancreatic ductal adenocarcinoma cell line, MIA PaCa-2 with RalGAPβ deficiency or not, and identified distinct classes of Ral activation-related mRNA.

2023-04-24 | GSE223382 | GEO

LYSET/TMEM251 KO secretome from MIA PaCa-2 cells

Project description:Analysis of proteins secreted over 24 h in OptiMEM by LYSET/TMEM251 knockout and control MIA PaCa-2 cells.

2022-09-29 | PXD029658 | Pride

RNA expression analysis after Mia PaCa 2 cell treatment with demethylating agent 5-Aza-2’-deoxycitidine (5-Aza)

Project description:Transcriptional profiling of Mia PaCa 2 cells treated with 5-Aza for 96 h. Relative abundance to untreated control cells was used to estimate the effect of DNA demethylation on the expression of the RNAs. Two-condition experiment, 5-Aza-treated vs. untretated Mia PaCa 2 cells. Biological replicates: 2. Technical replicates: 2.

2015-06-30 | E-GEOD-62959 | biostudies-arrayexpress

LYSET/TMEM251 SILAC Co-IP from MIA PaCA-2

Project description:Endogenous LYSET/TMEM251 was isolated via Co-IP from MIA PaCa-2 cells. LYSET KO cells were used as controls. Cells were grown in SILAC medium for 3 passages

2022-09-29 | PXD035821 | Pride

A PP2A-Integrator complex fine-tunes transcription by opposing CDK9 [ChIP-seq]

Project description:Gene expression by RNA Polymerase II (RNAPII) is tightly controlled by Cyclin-dependent kinases (CDKs) at discrete checkpoints during the transcription cycle. The RNAPII pausing checkpoint, engaged after transcription initiation, is controlled by CDK9 to regulate transcription in metazoans. We discovered that CDK9-mediated RNAPII pause-release is functionally opposed by a protein phosphatase 2A (PP2A) complex. PP2A dynamically competes for key CDK9 substrates, DSIF and RNAPII-CTD, and is recruited to transcription pausing sites by the Integrator complex subunit INTS6. INTS6 depletion confers resistance to CDK9 inhibition in a variety of normal and tumor cell lines. Loss of INTS6 abolishes the Integrator-PP2A association leading to unrestrained CDK9 activity, which amplifies transcriptional responses. Pharmacological PP2A activation synergizes with CDK9 inhibition to kill MLL-rearranged leukemias and solid tumors and provide therapeutic benefit in vivo. These data demonstrate that f inely-tuned gene expression relies on the balance of kinase and phosphatase activity at the pausing checkpoint.

2021-05-23 | GSE163804 | 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