Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Synergistic effects of Arid1a inactivation and oncogenic Kras mutation in mouse embryonic cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE207895 | GEO | 2022/09/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Synergistic effects of Arid1a inactivation and oncogenic Kras mutation in mouse embryonic cells

Project description:Synergistic effects of Arid1a inactivation and oncogenic Kras mutation in mouse embryonic cells

| PRJNA857642 | ENA

Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

Project description:To explore mechanisms underlying the cooperative effect in the proliferative phenotype, we harvest MEFs of different genotypes (KA, K, A, WT) recombined and un-recombined.

2022-09-05 | GSE207888 | GEO

Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

Project description:To explore transcriptomic mechanisms underlying the cooperative effect in the proliferative phenotype, we harvest MEFs of different genotypes (KA, K, A, WT) recombined and un-recombined. We performed RNA-seq analysis on 5 recombined (Ad-CMV-Cre) cell lines of each genotypic conditions (WT, Arid1a L/L , Kras-LSL-G12D, and Kras-LSL-G12D; Arid1a L/L) as well as 2 or 3 un-recombined (Ad-CMV-GFP) or mock-infected MEF cell lines.

2022-09-05 | GSE207891 | GEO

Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

Project description:Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

| PRJNA857645 | ENA

Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

Project description:Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

| PRJNA857592 | ENA

Arid1a in mouse embryonic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-24 | GSE140925 | GEO

A mouse model of melanoma driven by oncogenic KRAS.

Project description:The small G-protein NRAS is mutated in 22% of human melanomas, whereas the related proteins KRAS and HRAS are mutated in only 2% and 1% of melanomas, respectively. We have developed a mouse model of melanoma in which Cre recombinase/LoxP technology is used to drive inducible expression of (G12V)KRAS in the melanocytic lineage. The mice develop skin hyperpigmentation, nevi, and tumors that bear many of the cardinal histopathology features and molecular characteristics of human melanoma. These tumors invade and destroy the underlying muscles and cells derived from them can grow as subcutaneous tumors and colonize the lungs of nude mice. These data establish that oncogenic KRAS can be a founder event in melanomagenesis.

| S-EPMC2896549 | biostudies-literature

Immune modulatory effects of oncogenic KRAS in cancer.

Project description:Oncogenic KRAS mutations are the most frequent mutations in human cancer, but most difficult to target. While sustained proliferation caused by oncogenic KRAS-downstream signalling is a main driver of carcinogenesis, there is increasing evidence that it also mediates autocrine effects and crosstalk with the tumour microenvironment (TME). Here, we discuss recent reports connecting KRAS mutations with tumour-promoting inflammation and immune modulation caused by KRAS that leads to immune escape in the TME. We discuss the preclinical work on KRAS-induced inflammation and immune modulation in the context of currently ongoing clinical trials targeting cancer entities that carry KRAS mutations and strategies to overcome the oncogene-induced effects on the immune system.

| S-EPMC7595113 | biostudies-literature

Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction.

Project description:Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.

| S-EPMC8016361 | biostudies-literature

Oncogenic KRAS G12D mutation promotes dimerization through a second, phosphatidylserine-dependent interface: a model for KRAS oligomerization.

Project description:KRAS forms transient dimers and higher-order multimers (nanoclusters) on the plasma membrane, which drive MAPK signaling and cell proliferation. KRAS is a frequently mutated oncogene, and while it is well known that the most prevalent mutation, G12D, impairs GTP hydrolysis, thereby increasing KRAS activation, G12D has also been shown to enhance nanoclustering. Elucidating structures of dynamic KRAS assemblies on a membrane has been challenging, thus we have refined our NMR approach that uses nanodiscs to study KRAS associated with membranes. We incorporated paramagnetic relaxation enhancement (PRE) titrations and interface mutagenesis, which revealed that, in addition to the symmetric 'α-α' dimerization interface shared with wild-type KRAS, the G12D mutant also self-associates through an asymmetric 'α-β' interface. The 'α-β' association is dependent on the presence of phosphatidylserine lipids, consistent with previous reports that this lipid promotes KRAS self-assembly on the plasma membrane in cells. Experiments using engineered mutants to spoil each interface, together with PRE probes attached to the membrane or free in solvent, suggest that dimerization through the primary 'α-α' interface releases β interfaces from the membrane promoting formation of the secondary 'α-β' interaction, potentially initiating nanoclustering. In addition, the small molecule BI-2852 binds at a β-β interface, stabilizing a new dimer configuration that outcompetes native dimerization and blocks the effector-binding site. Our data indicate that KRAS self-association involves a delicately balanced conformational equilibrium between transient states, which is sensitive to disease-associated mutation and small molecule inhibitors. The methods developed here are applicable to biologically important transient interactions involving other membrane-associated proteins.

| S-EPMC8494122 | biostudies-literature

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