Point mutation causing constitutive signaling of CXCR2 leads to transforming activity similar to Kaposi's sarcoma herpesvirus-G protein- coupled receptor

Journal of Immunology

Volumn 163, Issue 4, 1999, Pages 2017-2022

  Burger, Meike ^a   Burger, Jan A ^b   Hoch, Robert C ^a   Oades, Zenaida ^a   Takamori, Hiroshi ^a   Schraufstatter, Ingrid U ^c  

^a SCRIPPS RESEARCH INSTITUTE   (United States)

^b UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^c La Jolla Institute for Experimental Medicine   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ASPARTIC ACID; CHEMOKINE RECEPTOR; CHEMOKINE RECEPTOR CXCR2; GUANINE NUCLEOTIDE BINDING PROTEIN; MUTANT PROTEIN; UNCLASSIFIED DRUG; VALINE;

AMINO ACID SUBSTITUTION; ANIMAL CELL; ARTICLE; CARCINOGENESIS; CELL PROLIFERATION; CELL STRAIN 3T3; CONTROLLED STUDY; HERPES VIRUS; KAPOSI SARCOMA; MALIGNANT TRANSFORMATION; MOUSE; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL;

3T3 CELLS; ACTINS; AGAR; AMINO ACID SEQUENCE; ANIMALS; CALCIUM; CELL DIVISION; CELL TRANSFORMATION, NEOPLASTIC; CHEMOKINES, CXC; CONTACT INHIBITION; HERPESVIRUS 8, HUMAN; HUMANS; INOSITOL PHOSPHATES; MICE; MOLECULAR SEQUENCE DATA; POINT MUTATION; RATS; RECEPTORS, CHEMOKINE; SARCOMA, KAPOSI; SIGNAL TRANSDUCTION; TUMOR CELLS, CULTURED;

EID: 0033566677     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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