|1.||Lau, Serrine S: 4 articles (11/2011 - 08/2002)|
|2.||Monks, Terrence J: 4 articles (11/2011 - 08/2002)|
|3.||Cohen, Jennifer D: 2 articles (11/2011 - 08/2011)|
|4.||Gard, Jaime M C: 1 article (11/2011)|
|5.||Dietrich, Justin D: 1 article (11/2011)|
|6.||Nagle, Raymond B: 1 article (11/2011)|
|7.||Tham, Kimberly Y: 1 article (08/2011)|
|8.||Gallegos, Alfred C: 1 article (08/2011)|
|9.||Mastrandrea, Nicholas J: 1 article (08/2011)|
|10.||Patel, Sonal K: 1 article (03/2003)|
08/01/2002 - "Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development. "
11/01/2011 - "Critical proteins in both pathways are activated following treatment of Eker rats (Tsc-2(EK/+)) with the nephrocarcinogen 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ), which also results in loss of the wild-type allele of Tsc-2 in renal preneoplastic lesions and tumors. "
03/01/2003 - "Treatment of wild-type (Tsc-2(+/+)) and mutant (Tsc-2(EK/+)) Eker rats with 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 7.5 micro mol/kg. i.v.), a potent redox active and nephrotoxic metabolite of hydroquinone increases the incidence of renal tumors only in animals carrying the mutant Tsc-2(EK/+) allele. "
08/01/2011 - "Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels. "
10/01/1995 - "Although, the activity of gamma-GT was similar in mice and guinea pigs, only guinea pigs were susceptible to 2,3,5-(triGSyl)HQ (200 micromol/kg iv)-induced renal necrosis. "
12/01/1992 - "Administration of 2,3,5-(triglutathion-S-yl)hydroquinone [2,3,5-(triGSyl)HQ] to rats causes severe renal proximal tubular necrosis. "
12/01/1992 - "A total collapse in RRM function occurred by 24 hr. The effects of 2,3,5-(triGSyl)HQ on state 4 respiration preceded significant elevations in blood urea nitrogen, which occurred at 8 hr. However, pretreatment of animals with probenecid, an inhibitor of organic anion transport, caused a significant decrease in the 2,3,5-(triGSyl)HQ-mediated elevations in state 4 respiration at 1 hr, without preventing the subsequent development of renal necrosis. "
|3.||Proteins (Proteins, Gene)
|6.||tuberous sclerosis complex 2 protein (tuberin)
|7.||hydroquinone (Black and White)