Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Evaluation of mutational changes in tumors arising in VilCre; KrasQ61R mice

ABSTRACT: We observed a number of small intestinal tumors arising in Kras Q61R animals. Here, we sought to determine if there are any mutations to explain the development of these tumors.

ORGANISM(S): Mus musculus

PROVIDER: GSE301556 | GEO | 2026/04/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Evaluation of mutational changes in tumors arising in VilCre KrasQ61R mice

Project description:Evaluation of mutational changes in tumors arising in VilCre KrasQ61R mice

| PRJNA1285449 | ENA

Expression of Kras isoforms in Kras-mutant conditional knock-in alleles.

Project description:We have generated a novel Kras-LSL-Q61R allele. Here, we aim to evaluate the expression of the Kras isoforms and if the mutant Kras alleles (G12D and Q61R) express similar levels to one another and Kras WT.

2026-04-05 | GSE301565 | GEO

RNAseq of genetically engineered mouse model (GEMM) tumors

Project description:We report the expression profiling of lung adenocarcinoma tumors arising from genetically engineered mice with activation of KRAS(K) and loss of either SMARCA4 (S), p53(P) or both.

2018-06-17 | GSE94927 | GEO

Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

Project description:Purpose: Evaluation of the impact of a reduction in Bptf levels on the nature of lymphomas arising from Em-Myc mice. Results: Bptf heterozygous tumors show reduced activity of the E2F and c-MYC pathways, together with increased activity of the NF-kB pathway.

2019-12-10 | GSE141647 | GEO

RNA-seq Analysis of KRAS Mutant HPNE Pancreatic Ductal Epithelial Cells

Project description:KRAS mutations drive pancreatic cancer initiation by reprogramming cellular signaling and the tumor microenvironment. Here, we investigate the early transcriptional impact of distinct KRAS mutants in a non-cancerous pancreatic epithelial context. Using RNA-seq, we profiled HPNE cells engineered with inducible KRAS variants (G12D, G12V, G12R, Q61H, Q61K, Q61R) compared to wild-type KRAS (WT) following 24-hour induction. This comparative analysis reveals that KRAS mutations differentially regulate immune and extracellular matrix remodeling pathways, with G12D and Q61R/H mutants driving pro-inflammatory signaling, while G12R and Q61k exhibits distinct transcriptional suppression. These findings highlight the mutation-specific transcriptional landscapes of KRAS in pancreatic epithelial cells and provide insight into the early events shaping the pancreatic tumor microenvironment.

2026-05-12 | GSE295683 | GEO

Dynamic conformational equilibria in the active states of KRas and NRas

Project description:The design of potent RAS inhibitors benefits from a molecular understanding of the dynamics in KRAS and NRAS and their oncogenic mutants. Here we characterize switch-1 dynamics in GTP-state KRAS and NRAS by 31P NMR, by 15N relaxation dispersion NMR, hydrogen-deuterium exchange mass spectrometry (HDX-MS), and molecular dynamics simulations. In GMPPNP-bound KRAS and NRAS, we see the co-existence of two conformational states, corresponding to an “inactive” state-1 and an “active” state-2, as previously reported. The KRAS oncogenic mutations G12D, G12C and G12V only slightly affect this equilibrium towards the “inactive” state-1, with rank order wt < G12C < G12D < G12V. In contrast, the NRAS Q61R oncogenic mutation shifts the equilibrium fully towards the “active” state-2. Our molecular dynamics simulations explain this by the observation of a transient hydrogen bond between the Arg61 side chain and the Thr35 backbone carbonyl oxygen. NMR relaxation dispersion experiments with GTP-bound KRAS Q61R confirm a drastic decrease in the population of state-1, but still detect a small residual population (1.8%) of this conformer. HDX-MS indicates that higher populations of state-1 correspond to increased hydrogen-deuterium exchange rates in some regions and increased flexibility, whereas low state-1 populations are associated with KRAS rigidification. We elucidated the mechanism of action of a potent KRAS G12D inhibitor, MRTX1133. Binding of this inhibitor to the switch-2 pocket causes a complete shift of KRAS G12D towards the “inactive” conformation and prevents binding of effector RAS-binding domain (RBD), by signaling through an allosteric network.

2025-05-07 | PXD054924 | Pride

Comparison of gene expression in cisplatin resistant tumors to chemonaive tumors from a lung cancer mouse model

Project description:Using a mouse model of non-small cell lung cancer driven by activated Kras and loss of p53 (KrasG12D;p53fl/fl), we sought to determine which genes change expression in the bulk tumor after repetitive treatment with cispatin. After tumors were treated multiple times with cisplatin and show no further response, we isolated RNA from tumors treated with cisplatin or a vehicle control (PBS) to determine which genes significantly change in expression in chemoresistant bulk tumors.

2021-11-11 | GSE135720 | GEO

U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations [RNA-Seq]

Project description:The mechanisms by which mutations of the splicing factor gene U2AF1 contribute to lung adenocarcinoma pathogenesis are not well understood. Here, we used prime editing to modify the endogenous U2AF1 gene in lung adenocarcinoma cells and assessed the resulting impact on alternative splicing. One specific KRAS mutation, G12S, leads to skipping of KRAS exon 2 and generation of a non-functional KRAS transcript. However, expression of the U2AF1 S34F mutant reverts this exon skipping and restores KRAS function, leading to an enrichment of U2AF1 S34F mutations in KRAS G12S-mutant lung adenocarcinomas. A comprehensive analysis of splicing factor/oncogene mutation co-occurrence in cancer genomes also revealed significant co-enrichment of KRAS Q61R and U2AF1 I24T mutations. Experimentally, KRAS Q61R mutation leads to KRAS exon 3 skipping, which in turn can be rescued by the expression of U2AF1 I24T. Our findings provide evidence that splicing factor mutations can rescue splicing defects caused by oncogenic mutations in a dynamic process of cascading selection.

2026-04-29 | GSE328821 | GEO

U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations

2026-04-29 | GSE328804 | GEO

Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

Project description:Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

| PRJNA594301 | ENA