Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Japanese urothelial (bladder, renal pelvis and ureter) cancer patients (n = 83) and community controls (n = 101) were compared for rates of polymorphism in exon 7 of the cytochrome P4501A1 (CYP1A1) gene or homozygous deletion of the glutathione S-transferase class mu (GSTM1) gene. A CYP1A1 polymorphism was detected in a HinCII polymorphism assay utilizing a primer with a single base pair mismatch. The frequency distribution of the CYP1A1 genotypes in urothelial cancer patients showed no significant difference from that in healthy controls. The increased frequency of homozygous deletions of GSTM1 gene loci in patients with urothelial cancer was statistically significant compared with the controls, 51 of 83 (61%) and 43 of 101 (43%) (odds ratio = .2.15, 95% confidence interval = 1.18-3.86). These results lead us to conclude that homozygous deletion of the GSTM1 gene may be associated with susceptibility to urothelial cancer.
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PMID:Cytochrome P4501A1 gene polymorphism and homozygous deletion of the glutathione S-transferase M1 gene in urothelial cancer patients. 769 28

The TBX18 transcription factor is a crucial developmental regulator of several organ systems in mice, and loss of its transcriptional repression activity causes dilative nephropathies in humans. The molecular complexes with which TBX18 regulates transcription are poorly understood prompting us to use an unbiased proteomic approach to search for protein interaction partners. Using overexpressed dual tagged TBX18 as bait, we identified by tandem purification and subsequent LC-MS analysis TBX18 binding proteins in 293 cells. Clustering of functional annotations of the identified proteins revealed a highly significant enrichment of transcriptional cofactors and homeobox transcription factors. Using nuclear recruitment assays as well as GST pull-downs, we validated CBFB, GAR1, IKZF2, NCOA5, SBNO2 and CHD7 binding to the T-box of TBX18 in vitro. From these transcriptional cofactors, CBFB, CHD7 and IKZF2 enhanced the transcriptional repression of TBX18, while NCOA5 and SBNO2 dose-dependently relieved it. All tested homeobox transcription factors interacted with the T-box of TBX18 in pull-down assays, with members of the Pbx and Prrx subfamilies showing coexpression with Tbx18 in the developing ureter of the mouse. In summary, we identified and characterized new TBX18 binding partners that may influence the transcriptional activity of TBX18 in vivo.
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PMID:Proteomic analysis identifies transcriptional cofactors and homeobox transcription factors as TBX18 binding proteins. 3007 Oct 41