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A comprehensive and quantitative interactome of RAS

ABSTRACT: We investigated a comprehensive and quantitative interactome of RAS, a protein found to be a driver of many human cancers. This resource identifies interactors of the active form of RAS (nucleotide-dependent) as well as isoform-specific (KRAS, HRAS, and NRAS) interactors of RAS. Several of the proteins identified were confirmed as being important for cancer cell viability and senescence.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Sheng Zhang

LAB HEAD: Sheng Zhang

PROVIDER: PXD034847 | Pride | 2022-10-13

REPOSITORIES: Pride

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A Proteomic Approach Identifies Isoform-Specific and Nucleotide-Dependent RAS Interactions.

Miller Seth P SP Maio George G Zhang Xiaoyu X Badillo Soto Felix S FS Zhu Julia J Ramirez Stephen Z SZ Lin Hening H

Molecular & cellular proteomics : MCP 20220714 8

Active mutations in the RAS genes are found in ∼30% of human cancers. Although thought to have overlapping functions, RAS isoforms show preferential activation in human tumors, which prompted us to employ a comparative and quantitative proteomics approach to generate isoform-specific and nucleotide-dependent interactomes of the four RAS isoforms, KRAS4A, KRAS4B, HRAS, and NRAS. Many isoform-specific interacting proteins were identified, including HRAS-specific CARM1 and CHK1 and KRAS-specific PI ...[more]

PMID: 35839996

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Interrogation of the oncogenic RAS interactomes by BirA* based proximity labeling

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Transcriptional targets of oncogenic RAS proteins that mediate their ability to induce cellular transformation

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2016-09-08 | E-GEOD-62827 | biostudies-arrayexpress

Oncogenic potential of RAS isoforms in melanocytes

Project description:We compared the transformation efficiencies of mutant NRAS and KRAS in immortal, non-transformed Ink4a/Arf-deficient melanocytes. NRAS mutation leads to increased cellular proliferation and is potently tumorigenic. In contrast, KRAS mutation does not enhance melanocyte proliferation and is only weakly tumorigenic on its own. While both NRAS and KRAS activate MAPK signaling, only NRAS enhances MYC activity in these cells. Our data suggests that the activity of specific RAS isoforms is context dependent and provides a possible explanation for the prevalence of NRAS mutations in melanoma.In addition, understanding this mechanism will have important implications for cancer therapies targeting RAS pathways. Keywords: RAS isoforms Common Reference

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BioID proximity biotinylation-MS analysis of human main RAS GTPases in K-562 CML cells

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Transcription profiling of human peripheral blood mononuclear cells WITH a germline NRAS mutation vs controls reveals NRAScauses a novel human autoimmune lymphoproliferative syndrome (ALPS)

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2008-04-04 | E-GEOD-7345 | biostudies-arrayexpress

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