Cell proliferation is insufficient, but loss of tuberin is necessary, for chemically induced nephrocarcinogenicity

American Journal of Physiology - Renal Physiology

Volumn 283, Issue 2 52-2, 2002, Pages

  Yoon, Hae Seong ^a   Monks, Terrence J ^a   Everitt, Jeffrey I ^b   Walker, Cheryl L ^c   Lau, Serrine S ^a  

^a UNIVERSITY OF TEXAS AT AUSTIN   (United States)

^b CIIT CENTERS FOR HEALTH RESEARCH   (United States)

^c UNIVERSITY OF TEXAS   (United States)

Author keywords

Carcinogenesis; Cell cycle; Kidney; Tsc2 gene

Indexed keywords

2,3,5 TRIS(GLUTATHION S YL)HYDROQUINONE; CYCLIN D1; HYDROQUINONE DERIVATIVE; MITOGEN ACTIVATED PROTEIN KINASE; TUBERIN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CARCINOGENESIS; CELL CYCLE; CELL PROLIFERATION; CONTROLLED STUDY; ENZYME ACTIVITY; GENE FUNCTION; KIDNEY; KIDNEY MEDULLA; KIDNEY TUMOR; MALE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; TUMOR SUPPRESSOR GENE;

EID: 0036068587     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.00261.2001     Document Type: Article

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