{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":49,"searchCount":0},"additional":{"omics_type":["Unknown"],"volume":["80(24)"],"submitter":["Mendoza JA"],"pubmed_abstract":["Mechanisms of cellular transformation associated with human papillomavirus type 5 (HPV5), which is responsible for skin carcinomas in epidermodysplasia verruciformis (EV) patients, are poorly understood. Using a yeast two-hybrid screening and molecular and cellular biology experiments, we found that HPV5 oncoprotein E6 interacts with SMAD3, a key component in the transforming growth factor beta1 (TGF-beta1) signaling pathway. HPV5 E6 inhibits SMAD3 transactivation by destabilizing the SMAD3/SMAD4 complex and inducing the degradation of both proteins. Interestingly, the E6 protein of nononcogenic EV HPV9 failed to interact with SMAD3, suggesting that downregulation of the TGF-beta1 signaling pathway could be a determinant in HPV5 skin carcinogenesis."],"journal":["Journal of virology"],"pagination":["12420-4"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1676262"],"repository":["biostudies-literature"],"pubmed_title":["Human papillomavirus type 5 E6 oncoprotein represses the transforming growth factor beta signaling pathway by binding to SMAD3."],"pmcid":["PMC1676262"],"pubmed_authors":["Jacob Y","Favre M","Cassonnet P","Mendoza JA"],"view_count":["49"],"additional_accession":[]},"is_claimable":false,"name":"Human papillomavirus type 5 E6 oncoprotein represses the transforming growth factor beta signaling pathway by binding to SMAD3.","description":"Mechanisms of cellular transformation associated with human papillomavirus type 5 (HPV5), which is responsible for skin carcinomas in epidermodysplasia verruciformis (EV) patients, are poorly understood. Using a yeast two-hybrid screening and molecular and cellular biology experiments, we found that HPV5 oncoprotein E6 interacts with SMAD3, a key component in the transforming growth factor beta1 (TGF-beta1) signaling pathway. HPV5 E6 inhibits SMAD3 transactivation by destabilizing the SMAD3/SMAD4 complex and inducing the degradation of both proteins. Interestingly, the E6 protein of nononcogenic EV HPV9 failed to interact with SMAD3, suggesting that downregulation of the TGF-beta1 signaling pathway could be a determinant in HPV5 skin carcinogenesis.","dates":{"release":"2006-01-01T00:00:00Z","publication":"2006 Dec","modification":"2024-10-15T05:04:01.133Z","creation":"2019-06-06T12:46:22Z"},"accession":"S-EPMC1676262","cross_references":{"pubmed":["17020941"],"doi":["10.1128/JVI.02576-05","10.1128/jvi.02576-05"]}}