Long-term exposure to nicotine, via Ras pathway, induces cyclin D1 to stimulate G1 cell cycle transition

Journal of Biological Chemistry

Volumn 280, Issue 8, 2005, Pages 6369-6379

  Chu, Michelle ^a   Guo, Jinjin ^a   Chen, Chang Yan ^a  

^a BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BIOCHEMISTRY; ENZYMES; PERTURBATION TECHNIQUES; PULMONARY DISEASES; TOBACCO; TUMORS;

CELL CYCLE; KINASE; RECEPTORS;

CELLS;

CYCLIN D1; MITOGEN ACTIVATED PROTEIN KINASE; NICOTINE; NICOTINIC RECEPTOR; RAF PROTEIN; RAS PROTEIN; TRANSCRIPTION FACTOR AP 1; TRANSCRIPTION FACTOR E2F;

ANIMAL CELL; ARTICLE; CARCINOGENESIS; CELL CYCLE; CELL CYCLE G1 PHASE; CONTROLLED STUDY; EPITHELIUM CELL; LONG TERM EXPOSURE; LUNG CANCER; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; PROTEIN INDUCTION; RETINOBLASTOMA; SIGNAL TRANSDUCTION; TOBACCO;

ANIMALS; CELL CYCLE; CELL CYCLE PROTEINS; CELL LINE; CYCLIN D1; DNA-BINDING PROTEINS; E2F TRANSCRIPTION FACTORS; EPITHELIAL CELLS; G1 PHASE; LUNG; MAP KINASE SIGNALING SYSTEM; MICE; NICOTINE; PROMOTER REGIONS (GENETICS); RAS PROTEINS; TRANS-ACTIVATION (GENETICS); TRANSCRIPTION FACTORS;

BIOCHEMISTRY; CELLS; ENZYMES; TOBACCO; TUMORS;

EID: 14844334141     PISSN: 00219258     EISSN: None     Source Type: Journal    
DOI: 10.1074/jbc.M408947200     Document Type: Article

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