ArticleNature communications2021
Oncogenic KRAS is dependent upon an EFR3A-PI4KA signaling axis for potent tumorigenic activity.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 49 citations in OpenAlex.
- Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026Article
- E-Syt1 recruits PI4KA to endoplasmic reticulum-plasma membrane junctions to enhance PI4P synthesis.Science China. Life sciences · 2026Article
- KRAS G12C and KRAS G12D respond to lipid metabolism in an allele-specific manner.Journal of lipid research · 2026Article
- Glycosphingolipids regulate phosphatidylserine transport machinery that operates at ER-PM contact sites.Nature communications · 2026Article
- AlphaFold3: A Transformer in Life Sciences.Current medicinal chemistry · 2026Review
- Development of an inhibitory TTC7B selective nanobody that blocks EFR3 recruitment of PI4KA.The Journal of biological chemistry · 2025Article
- Development of an inhibitory TTC7B selective nanobody that blocks EFR3 recruitment of PI4KA.bioRxiv : the preprint server for biology · 2025Article
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- circEFR3A promotes breast cancer progression by sponging miR-590-3p to upregulate androgen receptor expression.Oncology letters · 2025Article
- Phosphoinositide kinases in cancer: from molecular mechanisms to therapeutic opportunities.Nature reviews. Cancer · 2025Review
- A Potential Role of EFR3A in Human Disease States.Biomolecules · 2025Review
- Review
- TTC7B triggers the PI4KA-AKT1-RXRA-FTO axis and inhibits colon cancer cell proliferation by increasing RNA methylation.International journal of biological sciences · 2025Article
- Reversal of metformin's anti-proliferative effect in fission yeastnpj metabolic health and disease · 2025Article
- Molecular basis for plasma membrane recruitment of PI4KA by EFR3.Science advances · 2024Article
- Transcriptome-Wide Profiling of Nascent RNA in Neurons with Enriched H3K27ac Signal Elevates eRNA Identification Efficiency.ACS chemical neuroscience · 2024Article
- Article
- Molecular basis for plasma membrane recruitment of PI4KA by EFR3.bioRxiv : the preprint server for biology · 2024Article
- Cis- and trans-eQTL TWASs of breast and ovarian cancer identify more than 100 susceptibility genes in the BCAC and OCAC consortia.American journal of human genetics · 2024Article
- A comprehensive genetic map of cytokine responses in Lyme borreliosis.Nature communications · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The HRAS, NRAS, and KRAS genes are collectively mutated in a fifth of all human cancers. These mutations render RAS GTP-bound and active, constitutively binding effector proteins to promote signaling conducive to tumorigenic growth. To further elucidate how RAS oncoproteins signal, we mined RAS interactomes for potential vulnerabilities. Here we identify EFR3A, an adapter protein for the phosphatidylinositol kinase PI4KA, to preferentially bind oncogenic KRAS. Disrupting EFR3A or PI4KA reduces phosphatidylinositol-4-phosphate, phosphatidylserine, and KRAS levels at the plasma membrane, as well as oncogenic signaling and tumorigenesis, phenotypes rescued by tethering PI4KA to the plasma membrane. Finally, we show that a selective PI4KA inhibitor augments the antineoplastic activity of the KRAS
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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.