Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.2.19 (ubiquitin-protein ligase)
 799 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung cancers are a heterogeneous group of tumors broadly classified as small cell or non-small cell lung cancers. In each case, numerous DNA mutations precede tumor formation, resulting in the activation of growth stimulatory genes and the loss of tumor suppressor genes. The known cellular functions of the tumor suppressor genes most commonly affected in lung cancer are reviewed herein, including the retinoblastoma (Rb) gene on chromosome 13q14, the p53 gene on 17p13, and the cyclin-dependent kinase inhibitor (CDKN2) gene on 9p21. The chromosomal locations for other potential tumor suppressor genes are on chromosomes 3p, 9p, and 11p. Candidate genes in these regions include the von Hippel-Lindau (VHL) gene at 3p25, the ubiquitin-activating enzyme homologue (UBE1L at 3p21, the genes for the dinucleoside polyphosphate hydrolase FHIT and receptor protein-tyrosine phosphatase gamma PTPRG at 3p14.2, the genes for tropomyosin beta (TM1) and a talin homologue (talin) at 9p21, and the H-ras gene at 11p15.
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PMID:Hot spots for molecular genetic alterations in lung cancer. 989 Dec 28

Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1, aka PGP9.5) is an abundant, neuronal deubiquitinating enzyme that has also been suggested to possess E3 ubiquitin-protein ligase activity and/or stabilize ubiquitin monomers in vivo. Recent evidence implicates dysregulation of UCH-L1 in the pathogenesis and progression of human cancers. Although typically only expressed in neurons, high levels of UCH-L1 have been found in many nonneuronal tumors, including breast, colorectal, and pancreatic carcinomas. UCH-L1 has also been implicated in the regulation of metastasis and cell growth during the progression of nonsmall cell lung carcinoma, colorectal cancer, and lymphoma. Together these studies suggest UCH-L1 has a potent oncogenic role and drives tumor development. Conversely, others have observed promoter methylation-mediated silencing of UCH-L1 in certain tumor subtypes, suggesting a potential tumor suppressor role for UCH-L1. In this paper, we provide an overview of the evidence supporting the involvement of UCH-L1 in tumor development and discuss the potential mechanisms of action of UCH-L1 in oncogenesis.
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PMID:Ubiquitin C-terminal hydrolase l1 in tumorigenesis. 2281 13