The ShcA SH2 domain engages a 14-3-3/PI3′K signaling complex and promotes breast cancer cell survival
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T. Pawson | J. Ursini-Siegel | W. Muller | W. R. Hardy | D. Zuo | L. Podmore | C. Ling | Y. Zheng | C. Zhang | Y. Zheng | Tony Pawson | Josie Ursini-Siegel | Chen Ling | William J. Muller
[1] Dihua Yu,et al. Overexpression of 14-3-3ζ in cancer cells activates PI3K via binding the p85 regulatory subunit , 2011, Oncogene.
[2] C. Arteaga,et al. ErbB3 ablation impairs PI3K/Akt-dependent mammary tumorigenesis. , 2011, Cancer research.
[3] Huamin Wang,et al. 14-3-3sigma exerts tumor-suppressor activity mediated by regulation of COP1 stability. , 2011, Cancer research.
[4] T. Pawson,et al. Receptor tyrosine kinase signaling favors a protumorigenic state in breast cancer cells by inhibiting the adaptive immune response. , 2010, Cancer research.
[5] W. Muller,et al. A novel role for 14-3-3sigma in regulating epithelial cell polarity. , 2010, Genes & development.
[6] M. Hung,et al. 14-3-3zeta Cooperates with ErbB2 to promote ductal carcinoma in situ progression to invasive breast cancer by inducing epithelial-mesenchymal transition. , 2009, Cancer cell.
[7] D. Levy,et al. Identification of a Stat3-dependent transcription regulatory network involved in metastatic progression. , 2009, Cancer research.
[8] J. Petrik,et al. Reversibility and recurrence of IGF-IR-induced mammary tumors , 2009, Oncogene.
[9] K. Brown,et al. Unraveling Breast Cancer Heterogeneity Through Transcriptomic and Epigenomic Analysis , 2009, Annals of Surgical Oncology.
[10] Peter Hoffmann,et al. 14-3-3:Shc Scaffolds Integrate Phosphoserine and Phosphotyrosine Signaling to Regulate Phosphatidylinositol 3-Kinase Activation and Cell Survival* , 2009, Journal of Biological Chemistry.
[11] S. Dalal,et al. A novel pocket in 14-3-3epsilon is required to mediate specific complex formation with cdc25C and to inhibit cell cycle progression upon activation of checkpoint pathways. , 2009, Experimental cell research.
[12] Hua Guo,et al. 14-3-3zeta overexpression defines high risk for breast cancer recurrence and promotes cancer cell survival. , 2009, Cancer research.
[13] F. Tashiro,et al. A Novel Binding Factor of 14-3-3β Functions as a Transcriptional Repressor and Promotes Anchorage-independent Growth, Tumorigenicity, and Metastasis* , 2008, Journal of Biological Chemistry.
[14] J. Ladbury,et al. A phosphorylation-dependent gating mechanism controls the SH2 domain interactions of the Shc adaptor protein. , 2008, Journal of molecular biology.
[15] T. Pawson,et al. ShcA signalling is essential for tumour progression in mouse models of human breast cancer , 2008, The EMBO journal.
[16] D. Huntsman,et al. Elevated Expression of DecR1 Impairs ErbB2/Neu-Induced Mammary Tumor Development , 2007, Molecular and Cellular Biology.
[17] J. Fawcett,et al. Combinatorial ShcA Docking Interactions Support Diversity in Tissue Morphogenesis , 2007, Science.
[18] D. Sgroi,et al. p66 Shc and tyrosine-phosphorylated Shc in primary breast tumors identify patients likely to relapse despite tamoxifen therapy , 2006, Breast Cancer Research.
[19] J. Gray,et al. Copy number aberrations in mouse breast tumors reveal loci and genes important in tumorigenic receptor tyrosine kinase signaling. , 2005, Cancer research.
[20] P. Pelicci,et al. Cooperation and selectivity of the two Grb2 binding sites of p52Shc in T-cell antigen receptor signaling to Ras family GTPases and Myc-dependent survival , 2005, Oncogene.
[21] Kang Z. Liu,et al. A Role for 14-3-3τ in E2F1 Stabilization and DNA Damage-induced Apoptosis* , 2004, Journal of Biological Chemistry.
[22] Rakesh Kumar,et al. The role of adapter protein Shc in estrogen non-genomic action , 2004, Steroids.
[23] R. Cardiff,et al. Epidermal growth factor receptor-dependent activation of Gab1 is involved in ErbB-2-mediated mammary tumor progression , 2003, Oncogene.
[24] Jeffrey W Pollard,et al. Progression to malignancy in the polyoma middle T oncoprotein mouse breast cancer model provides a reliable model for human diseases. , 2003, The American journal of pathology.
[25] R. Bagdasaryan,et al. Shc proteins are strong, independent prognostic markers for both node-negative and node-positive primary breast cancer. , 2003, Cancer research.
[26] M. Moran,et al. Grb2 and Shc Adapter Proteins Play Distinct Roles in Neu (ErbB-2)-Induced Mammary Tumorigenesis: Implications for Human Breast Cancer , 2001, Molecular and Cellular Biology.
[27] B. Neel,et al. New Role for Shc in Activation of the Phosphatidylinositol 3-Kinase/Akt Pathway , 2000, Molecular and Cellular Biology.
[28] M. Welham,et al. Shc associates with the IL-3 receptor β subunit, SHIP and Gab2 following IL-3 stimulation , 2000 .
[29] T. Pawson,et al. Accelerated Mammary Tumor Development in Mutant Polyomavirus Middle T Transgenic Mice Expressing Elevated Levels of Either the Shc or Grb2 Adapter Protein , 1999, Molecular and Cellular Biology.
[30] J. Koland,et al. Mutation of a Shc Binding Site Tyrosine Residue in ErbB3/HER3 Blocks Heregulin-dependent Activation of Mitogen-activated Protein Kinase* , 1998, The Journal of Biological Chemistry.
[31] John N. Hutchinson,et al. Requirement for Both Shc and Phosphatidylinositol 3′ Kinase Signaling Pathways in Polyomavirus Middle T-Mediated Mammary Tumorigenesis , 1998, Molecular and Cellular Biology.
[32] M. Moran,et al. Distinct tyrosine autophosphorylation sites negatively and positively modulate neu-mediated transformation , 1997, Molecular and cellular biology.
[33] S. Fesik,et al. Binding Affinities of Tyrosine-phosphorylated Peptides to the COOH-terminal SH2 and NH-terminal Phosphotyrosine Binding Domains of Shc (*) , 1996, The Journal of Biological Chemistry.
[34] Tony Pawson,et al. The Shc adaptor protein is highly phosphorylated at conserved, twin tyrosine residues (Y239/240) that mediate protein–protein interactions , 1996, Current Biology.
[35] M. Shibuya,et al. A novel pathway from phosphorylation of tyrosine residues 239/240 of Shc, contributing to suppress apoptosis by IL‐3. , 1996, The EMBO journal.
[36] B. Margolis,et al. The phosphotyrosine interaction domain of Shc binds an LXNPXY motif on the epidermal growth factor receptor , 1995, Molecular and cellular biology.
[37] M. Kraus,et al. Cooperative signaling of ErbB3 and ErbB2 in neoplastic transformation and human mammary carcinomas. , 1995, Oncogene.
[38] T. Roberts,et al. Polyoma middle tumor antigen interacts with SHC protein via the NPTY (Asn-Pro-Thr-Tyr) motif in middle tumor antigen. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[39] Sheila M. Thomas,et al. Association of the Shc and Grb2/Sem5 SH2-containing proteins is implicated in activation of the Ras pathway by tyrosine kinases , 1992, Nature.
[40] B. Margolis,et al. Phosphatidylinositol 3′‐kinase is activated by association with IRS‐1 during insulin stimulation. , 1992, The EMBO journal.
[41] R. Cardiff,et al. Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease , 1992, Molecular and cellular biology.
[42] P. Leder,et al. Single-step induction of mammary adenocarcinoma in transgenic mice bearing the activated c-neu oncogene , 1988, Cell.
[43] B E Griffin,et al. Monoclonal antibodies against polyoma virus tumor antigens. , 1982, Proceedings of the National Academy of Sciences of the United States of America.
[44] D. Morrison,et al. The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development. , 2009, Trends in cell biology.
[45] M. Welham,et al. Shc associates with the IL-3 receptor beta subunit, SHIP and Gab2 following IL-3 stimulation. Contribution of Shc PTB and SH2 domains. , 2000, Cellular signalling.
[46] N. Asai,et al. The role of amino acids surrounding tyrosine 1062 in ret in specific binding of the shc phosphotyrosine-binding domain. , 1999, Endocrinology.