ArticleOncogene2004
Cbl-c suppresses v-Src-induced transformation through ubiquitin-dependent protein degradation.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- A TGF-β-responsive enhancer regulates SRC expression and epithelial-mesenchymal transition-associated cell migration.Journal of cell science · 2023Article
- Functional roles of SRC signaling in pancreatic cancer: Recent insights provide novel therapeutic opportunities.Oncogene · 2023Review
- Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis.Frontiers in oncology · 2023Article
- Proteomic Landscape of Extracellular Vesicles for Diffuse Large B-Cell Lymphoma Subtyping.International journal of molecular sciences · 2021Article
- Depletion of Csk preferentially reduces the protein level of LynA in a Cbl-dependent manner in cancer cells.Scientific reports · 2020Article
- Loss of function Cbl-c mutations in solid tumors.PloS one · 2019Article
- Article
- Activation of zebrafish Src family kinases by the prion protein is an amyloid-β-sensitive signal that prevents the endocytosis and degradation of E-cadherin/β-catenin complexes in vivo.Molecular neurodegeneration · 2016Article
- Src regulates cigarette smoke-induced ceramide generation via neutral sphingomyelinase 2 in the airway epithelium.American journal of respiratory cell and molecular biology · 2015Article
- Complementary genetic screens identify the E3 ubiquitin ligase CBLC, as a modifier of PARP inhibitor sensitivity.Oncotarget · 2015Article
- Article
- Endocytosis and the Src family of non-receptor tyrosine kinases.Biomolecular concepts · 2014Review
- CD2-associated protein (CD2AP) enhances casitas B lineage lymphoma-3/c (Cbl-3/c)-mediated Ret isoform-specific ubiquitination and degradation via its amino-terminal Src homology 3 domains.The Journal of biological chemistry · 2014Article
- Src-dependent Tks5 phosphorylation regulates invadopodia-associated invasion in prostate cancer cells.The Prostate · 2014Article
- Article
- Protein tyrosine kinase regulation by ubiquitination: critical roles of Cbl-family ubiquitin ligases.Biochimica et biophysica acta · 2013Review
- Article
- The N terminus of Cbl-c regulates ubiquitin ligase activity by modulating affinity for the ubiquitin-conjugating enzyme.The Journal of biological chemistry · 2010Article
- Alterations of ubiquitin ligases in human cancer and their association with the natural history of the tumor.Oncogene · 2009Article
- Restriction of Src activity by Cullin-5.Current biology : CB · 2009Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Cbl family proteins Cbl, Cbl-b, and Cbl-c/Cbl-3 are thought to regulate signaling through protein-tyrosine kinases, positively as scaffold proteins and negatively as ubiquitin ligases. However, the precise signaling pathways and target proteins for each Cbl family member are not well understood. Here we show that Src is a preferential target of Cbl-c for degradation. Although exogenous expression of all Cbl family proteins suppressed the anchorage-independent growth of v-Src-transformed NIH3T3 cells, only Cbl-c caused reversion of the refractile morphology. The level of v-Src protein was reduced by Cbl-c, possibly through a lysosome-dependent pathway. The TKB domain and RING finger of Cbl-c were important for its antioncogenic activity. Wild-type Cbl-c promoted ubiquitination of Src in 293T cells, whereas a RING finger mutant did not. Cbl-c bound specifically to Src phosphorylated at Tyr419. Furthermore, Cbl-c together with UbcH5 induced ubiquitination of Src in vitro. Importantly, the Tyr419 nonphosphorylated form of Src was not ubiquitinated by Cbl-c. Therefore, activated Src may be a direct target of Cbl-c in vivo. Our results suggest that Cbl and Cbl-b suppress v-Src-induced transformation through mechanisms distinct from that of Cbl-c.
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What OpenQuestion holds
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.