ArticleNature communications2018
Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 88 citations in OpenAlex.
- Dynamic remodeling of the KRAS interactome by direct RAS inhibitors with distinct mechanism of action reveals convergent responses.Oncogene · 2026Article
- A ternary association of KRas, EphA2, and integrins controls PDAC cell behavior.The Journal of biological chemistry · 2026Article
- Brief report: Therapeutic benefit of ISA-2011B in colorectal cancer.Molecular biology reports · 2026Article
- Proteomics- and BRET- screens identify SPRY2 as a Ras effector that impacts its membrane organization.iScience · 2025Article
- Intrinsic resistance to RAS inhibitors is driven by dysregulation of KRAS degradation.Nature communications · 2025Article
- Pancreatic Cells Are Resistant to KRASQ61L Expression due to Hyperactive ERK/MAPK Signaling and Apoptosis Induction.Cancer research communications · 2025Article
- Silicon-rhodamine-enabled identification for near-infrared light controlled proximity labeling in vitro and in vivo.Nature communications · 2025Article
- PIP5K1A Suppresses Ferroptosis and Induces Sorafenib Resistance by Stabilizing NRF2 in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Deciphering 17-β-hydroxysteroid dehydrogenase 4: from molecular insights to cancer therapeutics.Cancer cell international · 2025Review
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- Phosphoinositide kinases in cancer: from molecular mechanisms to therapeutic opportunities.Nature reviews. Cancer · 2025Review
- ATG9A vesicles are a subtype of intracellular nanovesicle.Journal of cell science · 2025Article
- The essential clathrin adapter protein complex-2 is tumor suppressive specifically in vivo.Nature communications · 2025Article
- Anti-proteolytic regulation of KRAS by USP9X/NDRG3 in KRAS-driven cancer development.Nature communications · 2025Article
- Rat Sarcoma Virus Family Genes in Acute Myeloid Leukemia: Pathogenetic and Clinical Implications.Biomedicines · 2025Review
- The small GTPase MRAS is a broken switch.Nature communications · 2025Article
- Article
- Functional and structural insights into RAS effector proteins.Molecular cell · 2024Review
- Oncogenic mutations of KRAS modulate its turnover by the CUL3/LZTR1 E3 ligase complex.Life science alliance · 2024Article
- Liprin-α1 contributes to oncogenic MAPK signaling by counteracting ERK activity.Molecular oncology · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In human cancers, oncogenic mutations commonly occur in the RAS genes KRAS, NRAS, or HRAS, but there are no clinical RAS inhibitors. Mutations are more prevalent in KRAS, possibly suggesting a unique oncogenic activity mediated by KRAS-specific interaction partners, which might be targeted. Here, we determine the specific protein interactomes of each RAS isoform by BirA proximity-dependent biotin identification. The combined interactomes are screened by CRISPR-Cas9 loss-of-function assays for proteins required for oncogenic KRAS-dependent, NRAS-dependent, or HRAS-dependent proliferation and censored for druggable proteins. Using this strategy, we identify phosphatidylinositol phosphate kinase PIP5K1A as a KRAS-specific interactor and show that PIP5K1A binds to a unique region in KRAS. Furthermore, PIP5K1A depletion specifically reduces oncogenic KRAS signaling and proliferation, and sensitizes pancreatic cancer cell lines to a MAPK inhibitor. These results suggest PIP5K1A as a potential target in KRAS signaling for the treatment of KRAS-mutant cancers.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.