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V-yes-1 Yamaguchi sarcoma viral oncogene homolog 1

c-Yes, YES1
This gene is the cellular homolog of the Yamaguchi sarcoma virus oncogene. The encoded protein has tyrosine kinase activity and belongs to the src family of proteins. This gene lies in close proximity to thymidylate synthase gene on chromosome 18, and a corresponding pseudogene has been found on chromosome 22. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Src, alpha-Synuclein, CAN, Lyn, V1a
Papers on c-Yes
Colon cancer cells escape 5FU chemotherapy-induced cell death by entering stemness and quiescence associated with the c-Yes/YAP axis.
Huet et al., Saint-Pierre-des-Corps, France. In Clin Cancer Res, Mar 2014
These quiescent cells overexpressed the tyrosine kinase c-Yes that became activated and membrane-associated upon 5FU exposure.
c-Yes tyrosine kinase is a potent suppressor of ES cell differentiation and antagonizes the actions of its closest phylogenetic relative, c-Src.
Smithgall et al., Pittsburgh, United States. In Acs Chem Biol, Feb 2014
Here we used ES cells to test the hypothesis that c-Src and its closest phylogenetic relative, c-Yes, act in biological opposition despite their strong homology.
YES1 activation elicited by heat stress is anti-apoptotic in mouse pachytene spermatocytes.
Li et al., Xi'an, China. In Biol Reprod, Dec 2013
Herein, YES1, a nonreceptor protein tyrosine kinase, was found to be significantly up-regulated in pachytene spermatocytes (PS) during early recovery from a transient testicular heat stress.
Identification of potent Yes1 kinase inhibitors using a library screening approach.
Davis et al., Frederick, United States. In Bioorg Med Chem Lett, Sep 2013
Yes1 kinase has been implicated as a potential therapeutic target in a number of cancers including melanomas, breast cancers, and rhabdomyosarcomas.
Individual Src-family tyrosine kinases direct the degradation or protection of the clock protein Timeless via differential ubiquitylation.
Smithgall et al., Pittsburgh, United States. In Cell Signal, Apr 2013
Here we report that mammalian Timeless is an SH3 domain-binding protein and substrate for several members of the Src protein-tyrosine kinase family, including Fyn, Hck, c-Src and c-Yes.
Investigation into mechanisms mediating the inhibitory effect of 1,4-benzodiazepines on mast cells by gene expression profiling.
Molderings et al., Bonn, Germany. In Life Sci, Apr 2013
Expression of the protein tyrosine kinases Lyn, Fgr and Yes1 was increased in HMC-1.2 cells as compared with the ontogenetically related HL60 cells.
TAF4b and TAF4 differentially regulate mouse embryonic stem cells maintenance and proliferation.
Dikstein et al., Israel. In Genes Cells, Mar 2013
Among them are the germ cell-specific transcription factor Sohlh2 and the protein kinase Yes1, which was recently shown to regulate ESC self-renewal.
c-Yes regulates cell adhesion at the apical ectoplasmic specialization-blood-testis barrier axis via its effects on protein recruitment and distribution.
Cheng et al., New York City, United States. In Am J Physiol Endocrinol Metab, Feb 2013
c-Yes, a nonreceptor protein tyrosine kinase belonging to the Src family kinases (SFKs) and a crucial signaling protein, was recently shown to be upregulated at the Sertoli cell-cell interface at the blood-testis barrier (BTB) at stages VIII-IX of the seminiferous epithelial cycle of spermatogenesis.
β-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis.
Hahn et al., Boston, United States. In Cell, 2013
Phosphorylation of YAP1 by the tyrosine kinase YES1 leads to localization of this complex to the promoters of antiapoptotic genes, including BCL2L1 and BIRC5.
LKB1/STK11 inactivation leads to expansion of a prometastatic tumor subpopulation in melanoma.
Sharpless et al., Chapel Hill, United States. In Cancer Cell, 2012
Results suggest that LKB1 inactivation in the context of RAS activation facilitates metastasis by inducing an SFK-dependent expansion of a prometastatic, CD24(+) tumor subpopulation.
The blood-testis barrier and its implications for male contraception.
Mruk et al., New York City, United States. In Pharmacol Rev, 2012
Studies have demonstrated that some unlikely partners, namely adhesion protein complexes (e.g., occludin-ZO-1, N-cadherin-β-catenin, claudin-5-ZO-1), steroids (e.g., testosterone, estradiol-17β), nonreceptor protein kinases (e.g., focal adhesion kinase, c-Src, c-Yes), polarity proteins (e.g., PAR6, Cdc42, 14-3-3), endocytic vesicle proteins (e.g., clathrin, caveolin, dynamin 2), and actin regulatory proteins (e.g., Eps8, Arp2/3 complex), are working together, apparently under the overall influence of cytokines (e.g., transforming growth factor-β3, tumor necrosis factor-α, interleukin-1α).
Array-based comparative genomic hybridization for genomic-wide screening of DNA copy number alterations in aggressive bone tumors.
Suzuki et al., Toyama, Japan. In J Exp Clin Cancer Res, 2011
On the other hand, NRAS, D2S447, RAF1, ROBO1, MYB, MOS, FGFR2, HRAS, D13S319, D13S327, D18S552, YES1 and DCC, were commonly low.
C-Src and c-Yes are two unlikely partners of spermatogenesis and their roles in blood-testis barrier dynamics.
Cheng et al., New York City, United States. In Adv Exp Med Biol, 2011
Src family kinases (SFKs), in particular c-Src and c-Yes, are nonreceptor protein tyrosine kinases that mediate integrin signaling at focal adhesion complex at the cell-extracellular matrix interface to regulate cell adhesion, cell cycle progression, cell survival, proliferation and differentiation, most notably in cancer cells during tumorigenesis and metastasis.
Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3.
Furukawa et al., United States. In J Biol Chem, 2011
Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3.
Regulation of mouse embryonic stem cell self-renewal by a Yes-YAP-TEAD2 signaling pathway downstream of LIF.
Annerén et al., Uppsala, Sweden. In J Cell Sci, 2011
YAP, TEAD2 and Yes are highly expressed in self-renewing embryonic stem cells, and are activated by LIF.
c-Yes regulates cell adhesion at the blood-testis barrier and the apical ectoplasmic specialization in the seminiferous epithelium of rat testes.
Cheng et al., New York City, United States. In Int J Biochem Cell Biol, 2011
c-Yes regulates blood-testis barrier and apical ectoplasmic specialization integrity by maintaining proper distribution of integral membrane proteins and actin filament organization at these sites
Specific oncogenic activity of the Src-family tyrosine kinase c-Yes in colon carcinoma cells.
Cruzalegui et al., Vitry-sur-Seine, France. In Plos One, 2010
c-Yes regulates specific oncogenic signalling pathways important for colon cancer progression that is not shared with c-Src.
c-Yes response to growth factor activation.
Flynn et al., Morgantown, United States. In Growth Factors, 2005
The most studied kinase of this nine member family, c-Src, shares a similar structure, as well as a similar expression pattern to that of another Src family protein, c-Yes.
Specificity in signaling by c-Yes.
Flynn et al., Morgantown, United States. In Front Biosci, 2003
This review summarizes the potential functions of c-Yes and its ability to modulate signals that are distinct from c-Src.
Expanding the role of NHERF, a PDZ-domain containing protein adapter, to growth regulation.
Shenolikar et al., Durham, United States. In Oncogene, 2001
NHERF also recruits non-membrane proteins such as the c-Yes/YAP-65 complex, members of the phospholipase Cbeta family and the GRK6A protein kinase to apical surface of polarized epithelial cells where they regulate or respond to membrane signals.
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