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Volumn 277, Issue 35, 2002, Pages 31768-31773

Deletion of the carboxyl terminus of Tie2 enhances kinase activity, signaling, and function: Evidence for an autoinhibitory mechanism

(3) Niu, Xi Lin a,b,c,d Peters, Kevin G a,b,c,d Kontos, Christopher D a,b,c,d

a Division of Cardiology (United States)

b DUKE UNIVERSITY MEDICAL CENTER (United States)

c PROCTER AND GAMBLE COMPANY (United States)

d DUKE UNIVERSITY (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CRYSTAL STRUCTURE; ENZYME INHIBITION; ENZYME KINETICS; SIGNALING; TUMORS;

MUTATIONS;

BIOCHEMISTRY;

ALKALINE PHOSPHATASE; FIBROBLAST GROWTH FACTOR RECEPTOR; GLUTATHIONE TRANSFERASE; HYBRID PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE; PHOSPHATIDYLINOSITOL; RECOMBINANT PROTEIN; TYROSINE KINASE RECEPTOR;

ANGIOGENESIS; ANIMAL CELL; APOPTOSIS; ARTICLE; CELL STRAIN 3T3; CONTROLLED STUDY; ENZYME ACTIVITY; IMMUNOPRECIPITATION; MOUSE; NONHUMAN; POLYACRYLAMIDE GEL ELECTROPHORESIS; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; TUMOR GROWTH;

3T3 CELLS; ANIMALS; BASE SEQUENCE; BINDING SITES; CELL LINE; DNA PRIMERS; GLUTATHIONE TRANSFERASE; KINETICS; MICE; PHOSPHORYLATION; PROTEIN CONFORMATION; RECEPTOR PROTEIN-TYROSINE KINASES; RECEPTOR, TIE-2; RECOMBINANT FUSION PROTEINS; SEQUENCE DELETION; SIGNAL TRANSDUCTION; SPODOPTERA; TRANSFECTION;

ANIMALIA;

EID: 0037200045 PISSN: 00219258 EISSN: None Source Type: Journal
DOI: 10.1074/jbc.M203995200 Document Type: Article

Times cited : (44)

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