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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE301565 | GEO | 2026/04/05

REPOSITORIES: GEO

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

Project description:Expression of Kras isoforms in Kras-mutant conditional knock-in alleles.

| PRJNA1285452 | ENA

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

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

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mRNA-seq of Myc and Yap1-activated mouse lung tumors and controls

Project description:mRNA-seq for expression profiling of Myc and Yap1 activated mouse lung tumors and controls. 4 cohorts of lung tumors induced through nasal instillation of Cre/sgRNA(MS2)-encoding lentivirus in mice carrying conditional P53 loss (P53 F/F), oncogenic Kras (Kras LSL-G12D/+), and CRISPRa/SAM construct (Rosa26(LSL-SAM) or YFP reporter (Rosa26(LSL-YFP): 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Myc) (PPKS/M); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Yap1) (PPKS/Y); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKS/NT); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-YFP) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKY/NT)

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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

FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer

Project description:Mutations in KRAS, particularly at codon 12, are frequent in adenocarcinomas of the colon, lungs and pancreas, driving carcinogenesis by altering cell signalling and reprogramming metabolism. However, the specific mechanisms by which different KRAS G12 alleles initiate distinctive patterns of metabolic reprogramming are unclear. Using isogenic panels of colorectal cell lines harbouring the G12A, G12C, G12D and G12V heterozygous mutations and employing transcriptomics, metabolomics, and extensive biochemical validation, we characterise distinctive features of each allele. We demonstrate that cells harbouring the common G12D and G12V oncogenic mutations significantly alter glutamine metabolism and nitrogen recycling through FOXO1-mediated regulation compared to parental lines. Moreover, with a combination of small molecule inhibitors targeting glutamine and glutamate metabolism, we also identify a common vulnerability that eliminates mutant cells selectively. These results highlight a previously unreported mutant-specific effect of KRAS alleles on metabolism and signalling that could be potentially harnessed for cancer therapy.

2025-08-28 | GSE306286 | GEO

Kras-induced ikk2/nf-kappaB activation by IL-1 alpha and p62 freedforward loops is required for development of pancreatic ductal adenocarcinoma

Project description:This SuperSeries is composed of the following subset Series: GSE27478: Gene expression differences between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice GSE33322: Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice Refer to individual Series

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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.

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