Receptor-independent G protein activation may account for the stimulatory effects of first-generation H1-receptor antagonists in HL-60 cells, basophils, and mast cells

Biochemical Pharmacology

Volumn 51, Issue 2, 1996, Pages 125-131

  Burde, Rahel ^a   Dippel, Edgar ^a   Seifert, Roland ^a,b  

^a CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

^b STANFORD UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Ca2+ influx; G proteins; H1 receptor antagonists; HL 60 leukemic cells; pertussis toxin; rat basophilic leukemia (RBL 2H3) cells

Indexed keywords

ADENOSINE 5' (N ETHYLCARBOXAMIDE); AMPHOPHILE; ANTIGEN; BUCLADESINE; CALCIUM; CATION; CHLORPHENIRAMINE; DIPHENHYDRAMINE; FORMYLMETHIONYLLEUCYLPHENYLALANINE; GUANINE NUCLEOTIDE BINDING PROTEIN; GUANOSINE 5' O (3 THIOTRIPHOSPHATE); GUANOSINE TRIPHOSPHATASE; HISTAMINE; HISTAMINE H1 RECEPTOR ANTAGONIST; PERTUSSIS TOXIN; PROMETHAZINE; RETINOIC ACID; SEROTONIN; TRANSDUCIN;

ANIMAL CELL; ARTICLE; BASOPHIL; CALCIUM MOBILIZATION; CALCIUM TRANSPORT; CELL ACTIVITY; CELL DIFFERENTIATION; CELL STRAIN HL 60; CONTROLLED STUDY; DRUG MECHANISM; HISTAMINE RELEASE; HUMAN; HUMAN CELL; HYDROLYSIS; LEUKEMIA CELL; MAST CELL; NONHUMAN; PRIORITY JOURNAL; RAT; SEROTONIN RELEASE;

EID: 0030069937     PISSN: 00062952     EISSN: None     Source Type: Journal    
DOI: 10.1016/0006-2952(95)02123-X     Document Type: Article

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