TIMP-2 upregulates RECK expression via dephosphorylation of paxillin tyrosine residues 31 and 118

Oncogene

Volumn 25, Issue 30, 2006, Pages 4230-4234

  Oh, J ^a   Diaz, T ^b   Wei, B ^b   Chang, H ^a   Noda, M ^c   Stetler Stevenson, W G ^b  

^a Korea University College of Medicine   (South Korea)

^b NATIONAL CANCER INSTITUTE   (United States)

^c KYOTO UNIVERSITY   (Japan)

Author keywords

Paxillin; Rac1; RECK; Src; TIMP 2

Indexed keywords

CRK LIKE PROTEIN; LYMPHOCYTE ANTIGEN RECEPTOR; MATRIX METALLOPROTEINASE INHIBITOR; PAXILLIN; PROTEIN TYROSINE KINASE; RAC1 PROTEIN; RAP1 PROTEIN; TISSUE INHIBITOR OF METALLOPROTEINASE 2; TYROSINE; VERY LATE ACTIVATION ANTIGEN 3;

ARTICLE; BINDING SITE; COMPLEX FORMATION; CONTROLLED STUDY; ENDOTHELIUM CELL; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; MICROVASCULATURE; PRIORITY JOURNAL; PROTEIN DEPHOSPHORYLATION; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; UPREGULATION;

CELLS, CULTURED; HUMANS; MEMBRANE GLYCOPROTEINS; PAXILLIN; PHOSPHORYLATION; RAC1 GTP-BINDING PROTEIN; RAP1 GTP-BINDING PROTEINS; SIGNAL TRANSDUCTION; SRC-FAMILY KINASES; TISSUE INHIBITOR OF METALLOPROTEINASE-2; TYROSINE; UP-REGULATION;

EID: 33646831912     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/sj.onc.1209444     Document Type: Article

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