A novel role for 14-3-3sigma in regulating epithelial cell polarity.
暂无分享,去创建一个
W. Muller | S. Muthuswamy | B. Xue | D. Zuo | C. Ling
[1] Qiutang Li,et al. 14-3-3sigma controls corneal epithelial cell proliferation and differentiation through the Notch signaling pathway. , 2010, Biochemical and biophysical research communications.
[2] 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.
[3] G. Mills,et al. Akt1 and akt2 play distinct roles in the initiation and metastatic phases of mammary tumor progression. , 2009, Cancer research.
[4] I. Macara,et al. The Par3/aPKC interaction is essential for end bud remodeling and progenitor differentiation during mammary gland morphogenesis. , 2009, Genes & development.
[5] Z. Xuan,et al. Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma , 2008, Cell.
[6] Stephen T. Brown,et al. An EGR2/CITED1 Transcription Factor Complex and the 14-3-3σ Tumor Suppressor Are Involved in Regulating ErbB2 Expression in a Transgenic-Mouse Model of Human Breast Cancer , 2007, Molecular and Cellular Biology.
[7] P. Sharp,et al. 14-3-3σ controls mitotic translation to facilitate cytokinesis , 2007, Nature.
[8] Marissa E. Nolan,et al. Par6–aPKC uncouples ErbB2 induced disruption of polarized epithelial organization from proliferation control , 2006, Nature Cell Biology.
[9] R. Zhao,et al. DNA damage-induced protein 14-3-3 sigma inhibits protein kinase B/Akt activation and suppresses Akt-activated cancer. , 2006, Cancer research.
[10] 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.
[11] I. Verma,et al. Identification of 14-3-3sigma mutation causing cutaneous abnormality in repeated-epilation mutant mouse. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[12] L. Siracusa,et al. A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice , 2005, Nature Genetics.
[13] John R Yates,et al. Targeted Proteomic Analysis of 14-3-3ς, a p53 Effector Commonly Silenced in Cancer*S , 2005, Molecular & Cellular Proteomics.
[14] R. Benton,et al. Drosophila PAR-1 and 14-3-3 Inhibit Bazooka/PAR-3 to Establish Complementary Cortical Domains in Polarized Cells , 2003, Cell.
[15] Hye Kyong Kweon,et al. Phosphorylation-Dependent Binding of 14-3-3 to the Polarity Protein Par3 Regulates Cell Polarity in Mammalian Epithelia , 2003, Current Biology.
[16] R. Cardiff,et al. Gene expression profiling of neu-induced mammary tumors from transgenic mice reveals genetic and morphological similarities to ErbB2-expressing human breast cancers. , 2003, Cancer research.
[17] T. Ried,et al. Centrosome abnormalities, recurring deletions of chromosome 4, and genomic amplification of HER2/neu define mouse mammary gland adenocarcinomas induced by mutant HER2/neu , 2002, Oncogene.
[18] O. Monni,et al. New amplified and highly expressed genes discovered in the ERBB2 amplicon in breast cancer by cDNA microarrays. , 2001, Cancer research.
[19] M. Bissell,et al. ErbB2, but not ErbB1, reinitiates proliferation and induces luminal repopulation in epithelial acini , 2001, Nature Cell Biology.
[20] J. Struewing,et al. MEDICINE AND , 2000 .
[21] Mong-Hong Lee,et al. Association of the Cyclin-dependent Kinases and 14-3-3 Sigma Negatively Regulates Cell Cycle Progression* , 2000, The Journal of Biological Chemistry.
[22] T. Pandita,et al. High frequency of hypermethylation at the 14-3-3 sigma locus leads to gene silencing in breast cancer. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[23] M. Rudnicki,et al. Amplification of the neu/erbB-2 oncogene in a mouse model of mammary tumorigenesis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[24] K. Kinzler,et al. 14-3-3σ is required to prevent mitotic catastrophe after DNA damage , 1999, Nature.
[25] R. Cardiff,et al. Elevated expression of activated forms of Neu/ErbB‐2 and ErbB‐3 are involved in the induction of mammary tumors in transgenic mice: implications for human breast cancer , 1999, The EMBO journal.
[26] S. Bull,et al. neu/erbB-2 amplification identifies a poor-prognosis group of women with node-negative breast cancer. Toronto Breast Cancer Study Group. , 1998, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[27] Y. Nakamura,et al. Allelic loss on chromosome 1p is Associated with progression and lymph node metastasis of primary breast carcinoma , 1998, Cancer.
[28] K. Kinzler,et al. 14-3-3σ Is a p53-Regulated Inhibitor of G2/M Progression , 1997 .
[29] P. Ravdin,et al. The c-erbB-2 proto-oncogene as a prognostic and predictive marker in breast cancer: a paradigm for the development of other macromolecular markers--a review. , 1995, Gene.
[30] N. Hynes,et al. The biology of erbB-2/neu/HER-2 and its role in cancer. , 1994, Biochimica et biophysica acta.
[31] M. Genuardi,et al. Distal deletion of chromosome Ip in ductal carcinoma of the breast. , 1989, American journal of human genetics.
[32] W Godolphin,et al. Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer. , 1989, Science.
[33] M. Hung,et al. 14-3-3 z Cooperates with ErbB2 to Promote Ductal Carcinoma In Situ Progression to Invasive Breast Cancer by Inducing Epithelial-Mesenchymal Transition , 2009 .
[34] F. Révillion,et al. Proteomic analysis reveals that 14-3-3σ is down-regulated in human breast cancer cells , 2001 .
[35] W. McGuire,et al. Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. , 1987, Science.