Expression of metalloproteinases and inhibitors in the differentiation of P19CL6 cells into cardiac myocytes.

[1]  G. Schultz,et al.  Expression analysis of the entire MMP and TIMP gene families during mouse tissue development , 2004, FEBS letters.

[2]  J. Saul,et al.  Myocardial remodeling after discrete radiofrequency injury: effects of tissue inhibitor of matrix metalloproteinase-1 gene deletion. , 2004, American journal of physiology. Heart and circulatory physiology.

[3]  Z. Galis,et al.  Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[4]  S. Tyagi,et al.  Matrix metalloproteinase activity expression in infarcted, noninfarcted and dilated cardiomyopathic human hearts , 1996, Molecular and Cellular Biochemistry.

[5]  V. Wee Yong,et al.  An Adverse Role for Matrix Metalloproteinase 12 after Spinal Cord Injury in Mice , 2003, The Journal of Neuroscience.

[6]  R. Schulz,et al.  Imbalance Between Tissue Inhibitor of Metalloproteinase-4 and Matrix Metalloproteinases During Acute Myoctardial Ischemia-Reperfusion Injury , 2003 .

[7]  Michael D. Schneider,et al.  A Wnt- and β-catenin-dependent pathway for mammalian cardiac myogenesis , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[8]  M. Kuzuya,et al.  Role of matrix metalloproteinases in vascular remodeling. , 2003, Journal of atherosclerosis and thrombosis.

[9]  Gillian Murphy,et al.  Metalloproteinase inhibitors: biological actions and therapeutic opportunities , 2002, Journal of Cell Science.

[10]  R. Kitsis,et al.  Microarray analysis of global changes in gene expression during cardiac myocyte differentiation. , 2002, Physiological genomics.

[11]  G. Schultz,et al.  Identification of an initiator-like element essential for the expression of the tissue inhibitor of metalloproteinases-4 (Timp-4) gene. , 2002, The Biochemical journal.

[12]  P. Brauer,et al.  Expression of tissue inhibitor of metalloproteinases (TIMPs) during early cardiac development , 2002, Mechanisms of Development.

[13]  D. Sheppard,et al.  The integrin αvβ8 mediates epithelial homeostasis through MT1-MMP–dependent activation of TGF-β1 , 2002, The Journal of cell biology.

[14]  J. D’Armiento Matrix metalloproteinase disruption of the extracellular matrix and cardiac dysfunction. , 2002, Trends in cardiovascular medicine.

[15]  Z. Werb,et al.  New functions for the matrix metalloproteinases in cancer progression , 2002, Nature Reviews Cancer.

[16]  Hiroshi Asanuma,et al.  Cardiac hypertrophy is inhibited by antagonism of ADAM12 processing of HB-EGF: Metalloproteinase inhibitors as a new therapy , 2002, Nature Medicine.

[17]  Wanmin Song,et al.  Degradation of type IV collagen by matrix metalloproteinases is an important step in the epithelial-mesenchymal transformation of the endocardial cushions. , 2000, Developmental biology.

[18]  J. D’Armiento,et al.  Disruption of the myocardial extracellular matrix leads to cardiac dysfunction. , 2000, The Journal of clinical investigation.

[19]  J. Quigley,et al.  MMP‐2 expression during early avian cardiac and neural crest morphogenesis , 2000, The Anatomical record.

[20]  A. Luttun,et al.  Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure , 1999, Nature Medicine.

[21]  R. Beddington,et al.  Axis Development and Early Asymmetry in Mammals , 1999, Cell.

[22]  S. Mckercher,et al.  Defective trophoblast function in mice with a targeted mutation of Ets2. , 1998, Genes & development.

[23]  P. McGuire,et al.  Spatial and temporal expression of the 72‐kDa type IV collagenase (MMP‐2) correlates with development and differentiation of valves in the embryonic avian heart , 1997, Developmental dynamics : an official publication of the American Association of Anatomists.

[24]  C. López-Otín,et al.  Structural analysis and promoter characterization of the human collagenase-3 gene (MMP13). , 1997, Genomics.

[25]  S. Kumar,et al.  Differential gene expression of extracellular matrix components in dilated cardiomyopathy , 1996, Journal of cellular biochemistry.

[26]  G. Butler,et al.  The Soluble Catalytic Domain of Membrane Type 1 Matrix Metalloproteinase Cleaves the Propeptide of Progelatinase A and Initiates Autoproteolytic Activation , 1996, The Journal of Biological Chemistry.

[27]  T Trusk,et al.  Epithelial-mesenchymal transformations in early avian heart development. , 1996, Acta anatomica.

[28]  A. Habara-Ohkubo Differentiation of beating cardiac muscle cells from a derivative of P19 embryonal carcinoma cells. , 1996, Cell structure and function.

[29]  J. O'Connell,et al.  Regulation of Matrix Metalloproteinase Activity a , 1994, Annals of the New York Academy of Sciences.

[30]  V. García-Martínez,et al.  Primitive-streak origin of the cardiovascular system in avian embryos. , 1993, Developmental Biology.

[31]  B. Wasylyk,et al.  The collagenase gene promoter contains a TPA and oncogene‐responsive unit encompassing the PEA3 and AP‐1 binding sites. , 1990, The EMBO journal.

[32]  B. Hogan,et al.  Developmental expression of tissue inhibitor of metalloproteinase (TIMP) RNA. , 1989, Development.

[33]  M. Kirby Cardiac Morphogenesis—Recent Research Advances , 1987, Pediatric Research.

[34]  M. McBurney,et al.  Control of muscle and neuronal differentiation in a cultured embryonal carcinoma cell line , 1982, Nature.