ArticleMolecular and cellular biology2002
v-Crk activates the phosphoinositide 3-kinase/AKT pathway by utilizing focal adhesion kinase and H-Ras.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 73 citations in OpenAlex.
- Natural product-derived icaritin exerts anti-glioblastoma effects by positively modulating estrogen receptor β.Experimental and therapeutic medicine · 2020Article
- Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1.Science signaling · 2018Article
- Identification and characterisation of a Theileria annulata proline-rich microtubule and SH3 domain-interacting protein (TaMISHIP) that forms a complex with CLASP1, EB1, and CD2AP at the schizont surface.Cellular microbiology · 2018Article
- Identification of Novel Crk-associated Substrate (p130Cas) Variants with Functionally Distinct Focal Adhesion Kinase Binding Activities.The Journal of biological chemistry · 2015Article
- Article
- Poldip2 controls vascular smooth muscle cell migration by regulating focal adhesion turnover and force polarization.American journal of physiology. Heart and circulatory physiology · 2014Article
- Identification and functional characterization of p130Cas as a substrate of protein tyrosine phosphatase nonreceptor 14.Oncogene · 2013Article
- Models of crk adaptor proteins in cancer.Genes & cancer · 2012Article
- HijAkt: The PI3K/Akt pathway in virus replication and pathogenesis.Progress in molecular biology and translational science · 2012Review
- Activation of a pro-survival pathway IL-6/JAK2/STAT3 contributes to glial fibrillary acidic protein induction during the cholera toxin-induced differentiation of C6 malignant glioma cells.Molecular oncology · 2011Article
- Targeting oncogenic miR-335 inhibits growth and invasion of malignant astrocytoma cells.Molecular cancer · 2011Article
- Proteins that bind the Src homology 3 domain of CrkI have distinct roles in Crk transformation.Oncogene · 2010Article
- From Hen House to Bedside: Tracing Hanafusa's Legacy from Avian Leukemia Viruses to SRC to ABL and Beyond.Genes & cancer · 2010Article
- Rac1-dependent intracellular superoxide formation mediates vascular endothelial growth factor-induced placental angiogenesis in vitro.Endocrinology · 2010Article
- Focal adhesion kinase: a prominent determinant in breast cancer initiation, progression and metastasis.Cancer letters · 2010Review
- Oscillatory flow-induced proliferation of osteoblast-like cells is mediated by alphavbeta3 and beta1 integrins through synergistic interactions of focal adhesion kinase and Shc with phosphatidylinositol 3-kinase and the Akt/mTOR/p70S6K pathway.The Journal of biological chemistry · 2010Article
- Focal adhesion kinase regulates pathogen-killing capability and life span of neutrophils via mediating both adhesion-dependent and -independent cellular signals.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Expression of a phosphorylated p130(Cas) substrate domain attenuates the phosphatidylinositol 3-kinase/Akt survival pathway in tamoxifen resistant breast cancer cells.Journal of cellular biochemistry · 2009Article
- Effects of celecoxib and ly117018 combination on human breast cancer cells in vitro.Breast cancer : basic and clinical research · 2009Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
v-Crk, an oncogene product of avian sarcoma virus CT10, efficiently transforms chicken embryo fibroblasts (CEF). We have recently reported that constitutive activation of the phosphoinositide 3-kinase (PI3K)/AKT pathway plays a critical role in the v-Crk-induced transformation of CEF. In the present study we investigated the molecular mechanism by which v-Crk activates the PI3K/AKT pathway. First, we found that v-Crk promotes the association of the p85 regulatory subunit of PI3K with focal adhesion kinase (FAK) by inducing the phosphorylation of the Y397 residue in FAK. This FAK phosphorylation needs activation of the Src family tyrosine kinase(s) for which the v-Crk SH2 domain is responsible. v-Crk was unable to activate the PI3K/AKT pathway in FAK-null cells, indicating the functional importance of FAK. In addition, we found that H-Ras is also required for the activation of the PI3K/AKT pathway. The v-Crk-induced activation of AKT was greatly enhanced by the overexpression of H-Ras or its guanine nucleotide exchange factor mSOS, which binds to the v-Crk SH3 domain, whereas a dominant-negative mutant of H-Ras almost completely suppressed this activation. Furthermore, we showed that v-Crk stimulates the interaction of H-Ras with the Ras binding domain in the PI3K p110 catalytic subunit. Our data indicated that the v-Crk-induced activation of PI3K/AKT pathway was cooperatively achieved by two distinct interactions. One is the interaction of p85 with tyrosine-phosphorylated FAK promoted by the v-Crk SH2 domain, and another is the interaction of p110 with H-Ras dictated by the v-Crk SH3 domain.
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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.