Modification of GATA-2 transcriptional activity in endothelial cells by the SUMO E3 ligase PIASy

Circulation Research

Volumn 92, Issue 11, 2003, Pages 1201-1208

  Chun, Tae Hwa ^a,c,d   Itoh, Hiroshi ^a   Subramanian, Lalitha ^b   Iñiguez Lluhí, Jorge A ^b   Nakao, Kazuwa ^a  

^a KYOTO UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^b UNIVERSITY OF MICHIGAN HEALTH SYSTEM   (United States)

^c UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

^d NONE   (United States)

Author keywords

Endothelin 1; GATA 2; PIAS family; SUMO ligase

Indexed keywords

ANGIOGENIC FACTOR; ENDOTHELIN 1; LIGASE; MESSENGER RNA; PROTEIN INHIBITOR OF ACTIVATED STAT; SUMO 1 PROTEIN; SUMO 2 PROTEIN; SUMO PROTEIN; TRANSCRIPTION FACTOR GATA 2; UNCLASSIFIED DRUG; CARRIER PROTEIN; DNA BINDING PROTEIN; GATA2 PROTEIN, HUMAN; GATA2 PROTEIN, MOUSE; PIAS4 PROTEIN, HUMAN; SIGNAL PEPTIDE; TRANSCRIPTION FACTOR; UBIQUITIN PROTEIN LIGASE;

AMINO TERMINAL SEQUENCE; ANIMAL CELL; ANIMAL TISSUE; ARTICLE; BLOOD VESSEL WALL; CARBOXY TERMINAL SEQUENCE; CELL SPECIFICITY; CONTROLLED STUDY; EMBRYO; ENDOTHELIUM CELL; ENZYME ACTIVITY; GENE EXPRESSION; GENE EXPRESSION REGULATION; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN FAMILY; PROTEIN PROTEIN INTERACTION; ANIMAL; BINDING SITE; BIOSYNTHESIS; C57BL MOUSE; CELL CULTURE; CELL LINE; CELL STRAIN COS1; DRUG ANTAGONISM; ENZYMOLOGY; GENE SILENCING; GENETICS; HELA CELL; METABOLISM; PHYSIOLOGY; TRANSACTIVATION; VASCULAR ENDOTHELIUM;

ANIMALS; BINDING SITES; CARRIER PROTEINS; CELL LINE; CELLS, CULTURED; COS CELLS; DNA-BINDING PROTEINS; ENDOTHELIN-1; ENDOTHELIUM, VASCULAR; GATA2 TRANSCRIPTION FACTOR; GENE SILENCING; HELA CELLS; HUMANS; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; LIGASES; MICE; MICE, INBRED C57BL; PROMOTER REGIONS (GENETICS); PROTEIN INHIBITORS OF ACTIVATED STAT; RNA, MESSENGER; SMALL UBIQUITIN-RELATED MODIFIER PROTEINS; TRANS-ACTIVATION (GENETICS); TRANSCRIPTION FACTORS; UBIQUITIN-PROTEIN LIGASES;

EID: 0038380273     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.0000076893.70898.36     Document Type: Article

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