ArticleMolecular and cellular biology2000
Regulation of c-SRC activity and function by the adapter protein CAS.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 129 citations in OpenAlex.
- Mechanism of beta-arrestin 1 mediated Src activation via Src SH3 domain revealed by cryo-electron microscopy.Nature communications · 2026Article
- Mechanism of beta-arrestin 1 mediated Src activation via Src SH3 domain revealed by cryo-electron microscopy.bioRxiv : the preprint server for biology · 2025Article
- Current understanding of PEAK family members in regulation of cellular signaling pathways and cancer therapy.Molecular and cellular biochemistry · 2025Review
- Deciphering the Role of BCAR3 in Cancer Progression: Gene Regulation, Signal Transduction, and Therapeutic Implications.Cancers · 2024Review
- Structural mapping of PEAK pseudokinase interactions identifies 14-3-3 as a molecular switch for PEAK3 signaling.Nature communications · 2023Article
- Activation of oncogenic tyrosine kinase signaling promotes insulin receptor-mediated cone photoreceptor survival.Oncotarget · 2016Article
- A Kinase-Independent Function of c-Src Mediates p130Cas Phosphorylation at the Serine-639 Site in Pressure Overloaded Myocardium.Journal of cellular biochemistry · 2015Article
- A novel role for ezrin in breast cancer angio/lymphangiogenesis.Breast cancer research : BCR · 2014Article
- SRChing for the substrates of Src.Oncogene · 2014Review
- Physical biology in cancer. 4. Physical cues guide tumor cell adhesion and migration.American journal of physiology. Cell physiology · 2014Review
- Article
- Src binds cortactin through an SH2 domain cystine-mediated linkage.Journal of cell science · 2012Article
- Lack of Csk-mediated negative regulation in a unicellular SRC kinase.Biochemistry · 2012Article
- The proto-oncogene c-src is involved in primordial follicle activation through the PI3K, PKC and MAPK signaling pathways.Reproductive biology and endocrinology : RB&E · 2012Article
- Breast cancer anti-estrogen resistance 3 (BCAR3) protein augments binding of the c-Src SH3 domain to Crk-associated substrate (p130cas).The Journal of biological chemistry · 2012Article
- NSP-CAS Protein Complexes: Emerging Signaling Modules in Cancer.Genes & cancer · 2012Article
- Cas and NEDD9 Contribute to Tumor Progression through Dynamic Regulation of the Cytoskeleton.Genes & cancer · 2012Article
- Src, p130Cas, and Mechanotransduction in Cancer Cells.Genes & cancer · 2012Article
- SRC points the way to biomarkers and chemotherapeutic targets.Genes & cancer · 2012Article
- Digitoxin and its analogs as novel cancer therapeutics.Experimental hematology & oncology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
SRC family kinases play essential roles in a variety of cellular functions, including proliferation, survival, differentiation, and apoptosis. The activities of these kinases are regulated by intramolecular interactions and by heterologous binding partners that modulate the transition between active and inactive structural conformations. p130(CAS) (CAS) binds directly to both the SH2 and SH3 domains of c-SRC and therefore has the potential to structurally alter and activate this kinase. In this report, we demonstrate that overexpression of full-length CAS in COS-1 cells induces c-SRC-dependent tyrosine phosphorylation of multiple endogenous cellular proteins. A carboxy-terminal fragment of CAS (CAS-CT), which contains the c-SRC binding site, was sufficient to induce c-SRC-dependent protein tyrosine kinase activity, as measured by tyrosine phosphorylation of cortactin, paxillin, and, to a lesser extent, focal adhesion kinase. A single amino acid substitution located in the binding site for the SRC SH3 domain of CAS-CT disrupted CAS-CT's interaction with c-SRC and inhibited its ability to induce tyrosine phosphorylation of cortactin and paxillin. Murine C3H10T1/2 fibroblasts that expressed elevated levels of tyrosine phosphorylated CAS and c-SRC-CAS complexes exhibited an enhanced ability to form colonies in soft agar and to proliferate in the absence of serum or growth factors. CAS-CT fully substituted for CAS in mediating growth in soft agar but was less effective in promoting serum-independent growth. These data suggest that CAS plays an important role in regulating specific signaling pathways governing cell growth and/or survival, in part through its ability to interact with and modulate the activity of c-SRC.
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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.