Differential expression of arrestins is a predictor of breast cancer progression and survival

[1]  Mina J Bissell,et al.  Normal and tumor-derived myoepithelial cells differ in their ability to interact with luminal breast epithelial cells for polarity and basement membrane deposition. , 2010, Journal of cell science.

[2]  Timothy Y. Huang,et al.  β-Arrestins Scaffold Cofilin with Chronophin to Direct Localized Actin Filament Severing and Membrane Protrusions Downstream of Protease-activated Receptor-2* , 2010, The Journal of Biological Chemistry.

[3]  H. Rui,et al.  Prolactin inhibits BCL6 expression in breast cancer through a Stat5a-dependent mechanism. , 2010, Cancer research.

[4]  J. Benovic,et al.  Non-visual Arrestins Are Constitutively Associated with the Centrosome and Regulate Centrosome Function* , 2010, The Journal of Biological Chemistry.

[5]  S. Lowe,et al.  Tumor suppressive functions of p53. , 2009, Cold Spring Harbor perspectives in biology.

[6]  J. Benovic,et al.  Identification of βArrestin2 as a corepressor of androgen receptor signaling in prostate cancer , 2009, Proceedings of the National Academy of Sciences.

[7]  H. Werner,et al.  The insulin-like growth factor-I receptor as an oncogene , 2009, Archives of physiology and biochemistry.

[8]  S. Saunier,et al.  Targeting of β-Arrestin2 to the Centrosome and Primary Cilium: Role in Cell Proliferation Control , 2008, PloS one.

[9]  R. Strieter,et al.  Depletion of β-Arrestin-2 Promotes Tumor Growth and Angiogenesis in a Murine Model of Lung Cancer1 , 2008, The Journal of Immunology.

[10]  Rongxi Yang,et al.  Rapid xenograft tumor progression in beta‐arrestin1 transgenic mice due to enhanced tumor angiogenesis , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  J. Benovic,et al.  Arrestin-2 Interacts with the Ubiquitin-Protein Isopeptide Ligase Atrophin-interacting Protein 4 and Mediates Endosomal Sorting of the Chemokine Receptor CXCR4* , 2007, Journal of Biological Chemistry.

[12]  G. Bokoch,et al.  β-Arrestin-dependent Regulation of the Cofilin Pathway Downstream of Protease-activated Receptor-2* , 2007, Journal of Biological Chemistry.

[13]  C. Lau,et al.  Differential effects of β-arrestins on the internalization, desensitization and ERK1/2 activation downstream of protease activated receptor-2 , 2007 .

[14]  Genee Y. Lee,et al.  The morphologies of breast cancer cell lines in three‐dimensional assays correlate with their profiles of gene expression , 2007, Molecular oncology.

[15]  G. Bokoch,et al.  Beta‐arrestin‐dependent regulation of the cofilin pathway downstream of Protease‐activated receptor‐2 , 2007, The Journal of biological chemistry.

[16]  Kathryn A DeFea,et al.  Stop that cell! Beta-arrestin-dependent chemotaxis: a tale of localized actin assembly and receptor desensitization. , 2007, Annual review of physiology.

[17]  R. Lefkowitz,et al.  β-Arrestins and Cell Signaling , 2007 .

[18]  S. Milano,et al.  Regulation of receptor trafficking by GRKs and arrestins. , 2007, Annual review of physiology.

[19]  J. Gutkind,et al.  G-protein-coupled receptors and cancer , 2007, Nature Reviews Cancer.

[20]  Wen-Lin Kuo,et al.  A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes. , 2006, Cancer cell.

[21]  D. Rimm,et al.  Classification of Breast Cancer Using Genetic Algorithms and Tissue Microarrays , 2006, Clinical Cancer Research.

[22]  Ping Wang,et al.  Protease-Activated Receptor-2 Simultaneously Directs β-Arrestin-1-Dependent Inhibition and Gαq-Dependent Activation of Phosphatidylinositol 3-Kinase† , 2006 .

[23]  C. Perou,et al.  Race, breast cancer subtypes, and survival in the Carolina Breast Cancer Study. , 2006, JAMA.

[24]  Qiong Shi,et al.  Role of β-arrestin 1 in the metastatic progression of colorectal cancer , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[25]  Douglas G Altman,et al.  Reporting recommendations for tumor marker prognostic studies. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[26]  Min Zhang,et al.  A Nuclear Function of β-Arrestin1 in GPCR Signaling: Regulation of Histone Acetylation and Gene Transcription , 2005, Cell.

[27]  O. Larsson,et al.  β-Arrestin Is Crucial for Ubiquitination and Down-regulation of the Insulin-like Growth Factor-1 Receptor by Acting as Adaptor for the MDM2 E3 Ligase* , 2005, Journal of Biological Chemistry.

[28]  Mina J. Bissell,et al.  Myoepithelial Cells: Their Origin and Function in Breast Morphogenesis and Neoplasia , 2005, Journal of Mammary Gland Biology and Neoplasia.

[29]  Hallgeir Rui,et al.  Ultrahigh density microarrays of solid samples , 2005, Nature Methods.

[30]  S. Doxsey,et al.  Centrosome control of the cell cycle. , 2005, Trends in cell biology.

[31]  W. Saunders.  Centrosomal amplification and spindle multipolarity in cancer cells. , 2005, Seminars in cancer biology.

[32]  R. Lefkowitz,et al.  Different G protein-coupled receptor kinases govern G protein and beta-arrestin-mediated signaling of V2 vasopressin receptor. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[33]  R. Lefkowitz,et al.  Constitutive Protease-activated Receptor-2-mediated Migration of MDA MB-231 Breast Cancer Cells Requires Both β-Arrestin-1 and -2* , 2004, Journal of Biological Chemistry.

[34]  D. Rimm,et al.  X-Tile , 2004, Clinical Cancer Research.

[35]  R. Lefkowitz.  Historical review: a brief history and personal retrospective of seven-transmembrane receptors. , 2004, Trends in pharmacological sciences.

[36]  W. Lingle,et al.  Centrosome Amplification and the Origin of Chromosomal Instability in Breast Cancer , 2004, Journal of Mammary Gland Biology and Neoplasia.

[37]  F. Balkwill.  The significance of cancer cell expression of the chemokine receptor CXCR4. , 2004, Seminars in cancer biology.

[38]  R. Lefkowitz,et al.  Reciprocal Regulation of Angiotensin Receptor-activated Extracellular Signal-regulated Kinases by β-Arrestins 1 and 2* , 2004, Journal of Biological Chemistry.

[39]  Lan Ge,et al.  A β-Arrestin-dependent Scaffold Is Associated with Prolonged MAPK Activation in Pseudopodia during Protease-activated Receptor-2-induced Chemotaxis* , 2003, Journal of Biological Chemistry.

[40]  R. Tibshirani,et al.  Repeated observation of breast tumor subtypes in independent gene expression data sets , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[41]  Yue Sun,et al.  β-Arrestin2 Is Critically Involved in CXCR4-mediated Chemotaxis, and This Is Mediated by Its Enhancement of p38 MAPK Activation* , 2002, The Journal of Biological Chemistry.

[42]  D. Rimm,et al.  Automated subcellular localization and quantification of protein expression in tissue microarrays , 2002, Nature Medicine.

[43]  F. Stivala,et al.  Amplified Centrosomes in Breast Cancer: A Potential Indicator of Tumor Aggressiveness , 2002, Breast Cancer Research and Treatment.

[44]  Robert J. Lefkowitz,et al.  Defective lymphocyte chemotaxis in β-arrestin2- and GRK6-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[45]  Carol Reynolds,et al.  Centrosome amplification drives chromosomal instability in breast tumor development , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[46]  G. Strous,et al.  β-Arrestin and Mdm2, Unsuspected Partners in Signaling from the Cell Surface , 2001, Science's STKE.

[47]  R. Tibshirani,et al.  Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[48]  G. Gimpl,et al.  The oxytocin receptor system: structure, function, and regulation. , 2001, Physiological reviews.

[49]  D. Morgan,et al.  Breast cancer , 2000, BMJ : British Medical Journal.

[50]  Christian A. Rees,et al.  Molecular portraits of human breast tumours , 2000, Nature.

[51]  Sandra,et al.  A dominant negative mutant of the insulin-like growth factor-I receptor inhibits the adhesion, invasion, and metastasis of breast cancer. , 1998, Cancer research.

[52]  N. Webster,et al.  Elevated insulin-like growth factor I receptor autophosphorylation and kinase activity in human breast cancer. , 1998, Cancer research.

[53]  E. Ginns,et al.  Oxytocin and milk removal are required for post-partum mammary-gland development. , 1997, Genes and function.

[54]  T. Insel,et al.  Oxytocin is required for nursing but is not essential for parturition or reproductive behavior. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[55]  A. Sapino,et al.  Oxytocin enhances myoepithelial cell differentiation and proliferation in the mouse mammary gland. , 1993, Endocrinology.

[56]  D. Yee,et al.  Insulin-like growth factors in human breast cancer , 1991, Breast Cancer Research and Treatment.

[57]  R Beuscart,et al.  Prognostic significance of insulin-like growth factor 1 receptors in human breast cancer. , 1990, Cancer research.

[58]  L. Luttrell.  Transmembrane signaling by G protein-coupled receptors. , 2006, Methods in molecular biology.

[59]  Qiong Shi,et al.  Role of beta-arrestin 1 in the metastatic progression of colorectal cancer. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[60]  T. Nielsen,et al.  MDM2 protein expression is a negative prognostic marker in breast carcinoma , 2006, Modern Pathology.

[61]  Lan Ma,et al.  A nuclear function of beta-arrestin1 in GPCR signaling: Regulation of histone acetylation and gene transcription (vol 123, pg 833, 2005) , 2006 .

[62]  Ping Wang,et al.  Protease-activated receptor-2 simultaneously directs beta-arrestin-1-dependent inhibition and Galphaq-dependent activation of phosphatidylinositol 3-kinase. , 2006, Biochemistry.

[63]  W. Lingle,et al.  Deregulation of the centrosome cycle and the origin of chromosomal instability in cancer. , 2005, Advances in experimental medicine and biology.

[64]  M. Ellis,et al.  Insulin-like growth factors in human breast cancer , 2004, Breast Cancer Research and Treatment.

[65]  R. Lefkowitz,et al.  Defective lymphocyte chemotaxis in beta-arrestin2- and GRK6-deficient mice. , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[66]  L. Donehower,et al.  Overexpression of Mdm 2 in mice reveals a p 53-independent role for Mdm 2 in tumorigenesis , 1998 .

[67]  J. Benovic,et al.  The role of receptor kinases and arrestins in G protein-coupled receptor regulation. , 1998, Annual review of pharmacology and toxicology.