Downregulation of Par-3 expression and disruption of Par complex integrity by TGF-beta during the process of epithelial to mesenchymal transition in rat proximal epithelial cells.

[1]  S. Atkinson,et al.  aPKC-PAR complex dysfunction and tight junction disassembly in renal epithelial cells during ATP depletion. , 2007, American journal of physiology. Cell physiology.

[2]  E. Hay,et al.  Cooperation between snail and LEF-1 transcription factors is essential for TGF-beta1-induced epithelial-mesenchymal transition. , 2006, Molecular biology of the cell.

[3]  V. Vasioukhin Faculty Opinions recommendation of Regulation of the polarity protein Par6 by TGFbeta receptors controls epithelial cell plasticity. , 2005 .

[4]  Yue Zhang,et al.  Regulation of the Polarity Protein Par6 by TGFß Receptors Controls Epithelial Cell Plasticity , 2005, Science.

[5]  I. Macara,et al.  Par-3 controls tight junction assembly through the Rac exchange factor Tiam1 , 2005, Nature Cell Biology.

[6]  F. Portillo,et al.  Transcriptional regulation of cadherins during development and carcinogenesis. , 2004, The International journal of developmental biology.

[7]  P. Dijke,et al.  New insights into TGF-β–Smad signalling , 2004 .

[8]  M. Ozawa,et al.  The transcription factor Snail downregulates the tight junction components independently of E-cadherin downregulation , 2004, Journal of Cell Science.

[9]  I. Macara Parsing the Polarity Code , 2004, Nature Reviews Molecular Cell Biology.

[10]  Youhua Liu Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. , 2004, Journal of the American Society of Nephrology : JASN.

[11]  J. Massagué,et al.  Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus , 2003, Cell.

[12]  J. Massagué,et al.  Mechanisms of TGF-beta signaling from cell membrane to the nucleus. , 2003, Cell.

[13]  A. Suzuki,et al.  Regulated protein–protein interaction between aPKC and PAR‐3 plays an essential role in the polarization of epithelial cells , 2002, Genes to cells : devoted to molecular & cellular mechanisms.

[14]  G. Joberty,et al.  Assembly of Epithelial Tight Junctions Is Negatively Regulated by Par6 , 2002, Current Biology.

[15]  A. Wodarz Establishing cell polarity in development , 2002, Nature Cell Biology.

[16]  Y. Nagai,et al.  PAR‐6 regulates aPKC activity in a novel way and mediates cell‐cell contact‐induced formation of the epithelial junctional complex , 2001, Genes to cells : devoted to molecular & cellular mechanisms.

[17]  Shoichiro Tsukita,et al.  Multifunctional strands in tight junctions , 2001, Nature Reviews Molecular Cell Biology.

[18]  T. Ohnishi,et al.  Atypical Protein Kinase C Is Involved in the Evolutionarily Conserved Par Protein Complex and Plays a Critical Role in Establishing Epithelia-Specific Junctional Structures , 2001, The Journal of cell biology.

[19]  E. Knust,et al.  Drosophila Atypical Protein Kinase C Associates with Bazooka and Controls Polarity of Epithelia and Neuroblasts , 2000, The Journal of cell biology.

[20]  G. Joberty,et al.  The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42 , 2000, Nature Cell Biology.

[21]  K. Kemphues,et al.  PARsing Embryonic Polarity , 2000, Cell.

[22]  J. Knoblich,et al.  DmPAR-6 directs epithelial polarity and asymmetric cell division of neuroblasts in Drosophila , 2000, Nature Cell Biology.

[23]  E. Knust,et al.  Control of spindle orientation in Drosophila by the Par-3-related PDZ-domain protein Bazooka , 1998, Current Biology.

[24]  James M. Anderson,et al.  Molecular architecture of tight junctions. , 1998, Annual review of physiology.

[25]  L. Shoshani,et al.  Role of tight junctions in establishing and maintaining cell polarity. , 1998, Annual review of physiology.

[26]  W. Birchmeier,et al.  Molecular aspects of mesenchymal-epithelial interactions. , 1993, Annual review of cell biology.

[27]  D. Morton,et al.  Identification of genes required for cytoplasmic localization in early C. elegans embryos , 1988, Cell.