ArticleOncogene2010
Anaplastic lymphoma kinase activates the small GTPase Rap1 via the Rap1-specific GEF C3G in both neuroblastoma and PC12 cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Research status and development trends of omics in neuroblastoma a bibliometric and visualization analysis.Frontiers in oncology · 2024Pooled it
- Anaplastic Lymphoma Kinase signaling stabilizes SLC3A2 expression via MARCH11 to promote neuroblastoma cell growth.Cell death and differentiation · 2024Article
- ALK F1174S mutation impairs ALK kinase activity in EML4-ALK variant 1 and sensitizes EML4-ALK variant 3 to crizotinib.Frontiers in oncology · 2023Article
- C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021Review
- C3G downregulation induces the acquisition of a mesenchymal phenotype that enhances aggressiveness of glioblastoma cells.Cell death & disease · 2021Article
- Protein Tyrosine Phosphatases in Neuroblastoma: Emerging Roles as Biomarkers and Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
- Expression of a novel brain specific isoform of C3G is regulated during development.Scientific reports · 2020Article
- Identification of the Wallenda JNKKK as an Alk suppressor reveals increased competitiveness of Alk-expressing cells.Scientific reports · 2020Article
- ALK Inhibitors-Induced M Phase Delay Contributes to the Suppression of Cell Proliferation.Cancers · 2020Article
- C3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formation.Cell communication and signaling : CCS · 2018Article
- Novel Mechanisms of ALK Activation Revealed by Analysis of the Y1278S Neuroblastoma Mutation.Cancers · 2017Article
- Crk-like adapter protein is overexpressed in cervical carcinoma, facilitates proliferation, invasion and chemoresistance, and regulates Src and Akt signaling.Oncology letters · 2016Article
- CRKL mediates EML4-ALK signaling and is a potential therapeutic target for ALK-rearranged lung adenocarcinoma.Oncotarget · 2016Article
- Oncogenic Signaling Adaptor Proteins.Journal of genetics and genomics = Yi chuan xue bao · 2015Review
- Article
- Unique genomic profile of fibrolamellar hepatocellular carcinoma.Gastroenterology · 2015Article
- The Ras-related protein, Rap1A, mediates thrombin-stimulated, integrin-dependent glioblastoma cell proliferation and tumor growth.The Journal of biological chemistry · 2014Article
- Article
- Neuroblastoma: developmental biology, cancer genomics and immunotherapy.Nature reviews. Cancer · 2013Review
- Cell culture and Drosophila model systems define three classes of anaplastic lymphoma kinase mutations in neuroblastoma.Disease models & mechanisms · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many different types of cancer originate from aberrant signaling from the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase (RTK), arising through different translocation events and overexpression. Further, activating point mutations in the ALK domain have been recently reported in neuroblastoma. To characterize signaling in the context of the full-length receptor, we have examined whether ALK is able to activate Rap1 and contribute to differentiation/proliferation processes. We show that ALK activates Rap1 via the Rap1-specific guanine-nucleotide exchange factor C3G, which binds in a constitutive complex with CrkL to activated ALK. The activation of the C3G/Rap1 pathway results in neurite outgrowth of PC12 cells, which is inhibited by either overexpression of Rap1GAP or siRNA-mediated knockdown of Rap1 itself or the guanine nucleotide exchange factor C3G. Significantly, this pathway also appears to function in the regulation of proliferation of neuroblastoma cells such as SK-N-SH and SH-SY5Y, because abrogation of Rap1 activity by Rap1-specific siRNA or overexpression of Rap1GAP reduces cellular growth. These results suggest that ALK activation of Rap1 may contribute to cell proliferation and oncogenesis of neuroblastoma driven by gain-of-function mutant ALK receptors.
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Registered trials
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.