ArticleOncogene2001
Regulation of Cbl phosphorylation by the Abl tyrosine kinase and the Nck SH2/SH3 adaptor.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 38 citations in OpenAlex.
- E3 ligase c-Cbl regulates intestinal inflammation through suppressing fungi-induced noncanonical NF-κB activation.Science advances · 2021Article
- Review
- Dynamic multi-site phosphorylation by Fyn and Abl drives the interaction between CRKL and the novel scaffolding receptors DCBLD1 and DCBLD2.The Biochemical journal · 2017Article
- Globularity and language-readiness: generating new predictions by expanding the set of genes of interest.Frontiers in psychology · 2014Article
- Direct regulation of nephrin tyrosine phosphorylation by Nck adaptor proteins.The Journal of biological chemistry · 2013Article
- Proteasomal degradation of Nck1 but not Nck2 regulates RhoA activation and actin dynamics.Nature communications · 2013Article
- The SH2 domain-containing proteins in 21 species establish the provenance and scope of phosphotyrosine signaling in eukaryotes.Science signaling · 2011Article
- 3BP2-deficient mice are osteoporotic with impaired osteoblast and osteoclast functions.The Journal of clinical investigation · 2011Article
- Functional cooperation between the proteins Nck and ADAP is fundamental for actin reorganization.Molecular and cellular biology · 2011Article
- ABL tyrosine kinases: evolution of function, regulation, and specificity.Science signaling · 2010Review
- Loss of c-abl facilitates anchorage-independent growth of p53- and RB- deficient primary mouse embryonic fibroblasts.Oncogene · 2004Article
- Cbl-ArgBP2 complex mediates ubiquitination and degradation of c-Abl.The Biochemical journal · 2003Article
- Roles of E3 ubiquitin ligases in cell adhesion and migration.Cell adhesion & migrationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The Cbl proto-oncogene product is tyrosine phosphorylated in response to a wide variety of stimuli. Cbl and the Abl nonreceptor tyrosine kinase both bind to SH3 domains from the SH2/SH3 adaptor Nck, and are candidate effectors for Nck function. Numerous additional SH2- and SH3-domain-mediated interactions are also possible between Cbl, Abl, and Nck. We find that these three signaling proteins associate when overexpressed in mammalian cells and can regulate each other's activity. Co-expression of wt Cbl together with c-Abl, the activity of which is normally repressed in vivo, led to extensive Abl-dependent phosphorylation of Cbl. The major proline-rich region of Cbl was required for its phosphorylation by c-Abl, but not by a constitutively activated Abl mutant, suggesting Cbl activates c-Abl by engaging its SH3 domain. Efficient phosphorylation of Cbl and its stable association with Abl required the SH2 domain of Abl, suggesting that SH2-phosphotyrosine interactions prevent dissociation of active Abl from Cbl. We also show that overexpression of Nck could repress the phosphorylation of Cbl by Abl in vivo. Studies with Nck mutants suggested that the Nck SH2 domain is responsible for inhibiting the activity of Abl toward both Cbl and Nck itself, most likely by competing with the Abl SH2 for tyrosine-phosphorylated binding sites.
Indexed as
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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.