ArticleNature communications2019
MERTK mediated novel site Akt phosphorylation alleviates SAV1 suppression.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- MERTK coordinates efferocytosis by regulating integrin localization and activation.Journal of cell science · 2026Article
- Genomic mapping reveals cisplatin disruption of protein phosphorylation signalling genome-wide.Metallomics : integrated biometal science · 2026Article
- cGAS Inhibits ALDH2 to Suppress Lipid Droplet Function and Regulate MASLD Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular mechanisms of Hippo pathway in tumorigenesis: therapeutic implications.Molecular biology reports · 2025Review
- AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024Review
- Article
- 2'3'-cGAMP interactome identifies 2'3'-cGAMP/Rab18/FosB signaling in cell migration control independent of innate immunity.Science advances · 2024Article
- Research progress of the Hippo signaling pathway in renal cell carcinoma.Asian journal of urology · 2024Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Review
- Co-targeting JAK1/STAT6/GAS6/TAM signaling improves chemotherapy efficacy in Ewing sarcoma.Nature communications · 2024Article
- Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma.Cell reports. Medicine · 2024Article
- TAM family kinases as therapeutic targets at the interface of cancer and immunity.Nature reviews. Clinical oncology · 2023Review
- Somatic gain-of-function mutations in BUD13 promote oncogenesis by disrupting Fbw7 function.The Journal of experimental medicine · 2023Article
- Development of VHL-recruiting STING PROTACs that suppress innate immunity.Cellular and molecular life sciences : CMLS · 2023Article
- STING Suppresses Mitochondrial VDAC2 to Govern RCC Growth Independent of Innate Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Synthesis and Initial Evaluation of MerTK Targeted PET Agents.Molecules (Basel, Switzerland) · 2022Article
- YAP1 and PRDM14 converge to promote cell survival and tumorigenesis.Developmental cell · 2022Article
- DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.Science signaling · 2022Article
- Constructing a novel prognostic signature of tumor driver genes for breast cancer.American journal of translational research · 2022Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
Akt plays indispensable roles in cell proliferation, survival and metabolism. Mechanisms underlying posttranslational modification-mediated Akt activation have been extensively studied yet the Akt interactome is less understood. Here, we report that SAV1, a Hippo signaling component, inhibits Akt, a function independent of its role in Hippo signaling. Binding to a proline-tyrosine motif in the Akt-PH domain, SAV1 suppresses Akt activation by blocking Akt's movement to plasma membrane. We further identify cancer-associated SAV1 mutations with impaired ability to bind Akt, leading to Akt hyperactivation. We also determine that MERTK phosphorylates Akt1-Y26, releasing SAV1 binding and allowing Akt responsiveness to canonical PI-3K pathway activation. This work provides a mechanism underlying MERTK-mediated Akt activation and survival signaling in kidney cancer. Akt activation drives oncogenesis and therapeutic resistance; this mechanism of Akt regulation by MERTK/SAV1 provides yet another complexity in an extensively studied pathway, and may yield prognostic information and therapeutic targets.
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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.