Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of vimentin deletion on gene expression in Kras-G12D-mutant, p53-null lung adenocarcinoma cells

ABSTRACT: Effect of vimentin deletion on gene expression in Kras-G12D-mutant, p53-null lung adenocarcinoma cells

PROVIDER: PRJNA933706 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23409826.fastq.gz	Fastqsanger.gz
	SRR23409827.fastq.gz	Fastqsanger.gz
	SRR23409828.fastq.gz	Fastqsanger.gz
	SRR23409829.fastq.gz	Fastqsanger.gz
	SRR23409830.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

KRAS-G12D drives immunosuppression in lung adenocarcinoma through paracrine signaling

Project description:Here, we sought to understand the KRAS-G12D-dependent changes occuring in the tumor and the tumor microenvironment within the lung.

2025-01-15 | GSE281744 | GEO

RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre;lsl-KRas[G12D] (KC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

Project description:Activation of endogenously expressed KRas[G12D] in the pancreas of mice gives rise primarily to early stage PanIN lesions, however such lesions can occasionally progress to end-stage ductal adenocarcinoma (PDAC). Progression of KRas[G12D]- initiated lesions to PDAC is accelerated by modest expression of MYC from the Rosa26 locus. Deletion of 1 copy of endogenous c-Myc or both copies of endogenous Zbtb17 (aka Miz1), slows progression to PDAC and extends healthful survival of Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC) mice. Tumours were removed from mice with all 4 genotypes and validated by histological examination prior to RNA-SEQ analysis.

2020-03-16 | E-MTAB-8797 | biostudies-arrayexpress

Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors

Project description:Breast Cancer (BC) has been associated with alterations in signaling through a number of growth factor and hormone regulated pathways. Mouse models for metastatic BC have been developed using oncoproteins that activate PI3K, Stat3 and Ras signaling. To determine the role of each pathway, we analyzed mouse mammary tumor formation when they were activated singly or pairwise. We used microarrays to detect differentially expressed genes in the KRas(G12D/+);CreT and R26(H1047R/+);KRas(G12D/+);CreT tumors Total RNA was extracted from tumors developed by Qiagen RNAeasy kit and hybridized on Affymetrix microarrays.

2015-09-16 | E-GEOD-73073 | biostudies-arrayexpress

RNA sequencing of SW1990 KRAS-G12D or KRAS-G12D/K128R knockin cell lines

Project description:RNA sequencing of SW1990 KRAS-G12D or KRAS-G12D/K128R knockin cell lines

| PRJNA1089940 | ENA

Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors

2015-09-16 | GSE73073 | GEO

Effect of vimentin deletion on gene expression in Kras-G12D-mutant, p53-null lung adenocarcinoma cells

Project description:Tumor initiation was induced in LSL-KrasG12D/+;Tp53flox/flox (KPV+/+) and LSL-KrasG12D/+;Tp53flox/flox;Vim-/- (KPV-/-) mice by Ad-cre delivery. Tumor cells were collected after 6 weeks and maintained in culture. RNA was collected from three independent cell lines per group and subjected to sequencing.

2023-05-31 | GSE225083 | GEO

Mutation-specific and common phosphotyrosine signatures of KRAS G12D and G13D alleles

Project description:KRAS is one of the most frequently mutated genes across all cancer subtypes. Two of the most frequent oncogenic KRAS mutations observed in patients result in glycine to aspartic acid substitution at either codon 12 (G12D) or 13 (G13D). Although the biochemical differences between these two predominant mutations are not fully understood, distinct clinical features of the resulting tumors suggest involvement of disparate signaling mechanisms. When we compared the global and phosphotyrosine proteomic profiles of isogenic colorectal cancer cell lines bearing either G12D or G13D KRAS mutation, we observed both shared as well as unique signaling events induced by the two KRAS mutations.

2021-06-09 | PXD009843 | Pride

KRAS WT and G12D overexpression RNA-seq

Project description:KRAS is an important oncogene in cancer. Long noncoding RNAs (lncRNAs) have been characterized to be involved in various types of cancer. In this study, we investigated the functions of KRAS-responsive lncRNAs in cancer. We perfomed the RNA-seq to examine the lncRNA expression after overexpession of KRAS WT and G12D in H1299 cells.

2020-12-17 | GSE124627 | GEO

RNA sequencing comparing mouse lung cancer cell lines derived from Kras G12D Trp53 -/- and Kras G12D Trp53 -/- sgMga tumors

Project description:The goal of this study was to compare expression profiles of mouse Kras G12D Trp53 -/- lung cancer cells that have inactivated MGA compared to controls

2020-11-17 | GSE161606 | GEO

Isogenic mouse model of Kras G12D mutation in Acute Lymphoblastic Leukemia

Project description:RAS-MAPK activating mutations in NRAS, KRAS and PTPN11 were present in 24/55 (44%) cases in our series of diangosis and relapsed ALL. To evaluate the specific role of RAS-MAPK activating mutations in chemotherapy resistance in ALL we used primary isogenic leukemia cells expressing either Kras wild type or a mutant oncogenic form of Kras (Kras G12D) Mechanistically, functional dissection of Kras wild type and mutant Kras (Kras G12D) isogenic ALL cells demonstrated induction of methotrexate resistance, but also improved response to vincristine, in mutant Kras-expressing ALL cells. These results pave the road for the development of tailored personalized therapies for the treatment of relapsed ALL

2018-11-01 | GSE75090 | 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