{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jha HC"],"funding":["NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","National Cancer Institute","NCI NIH HHS"],"pagination":["e1005801"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4963126"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(7)"],"pubmed_abstract":["Studies have suggested that Epithelial-Mesenchymal Transition (EMT) and transformation is an important step in progression to cancer. Par3 (partitioning-defective protein) is a crucial factor in regulating epithelial cell polarity. However, the mechanism by which the latency associated nuclear antigen (LANA) encoded by Kaposi's Sarcoma associated herpesvirus (KSHV) regulates Par3 and EMTs markers (Epithelial-Mesenchymal Transition) during viral-mediated B-cell oncogenesis has not been fully explored. Moreover, several studies have demonstrated a crucial role for EMT markers during B-cell malignancies. In this study, we demonstrate that Par3 is significantly up-regulated in KSHV-infected primary B-cells. Further, Par3 interacted with LANA in KSHV positive and LANA expressing cells which led"],"journal":["PLoS pathogens"],"pubmed_title":["KSHV-Mediated Regulation of Par3 and SNAIL Contributes to B-Cell Proliferation."],"pmcid":["PMC4963126"],"funding_grant_id":["R01 CA137894","R01 CA177423","P01 CA174439","P30 DK050306","P30-DK-050306","R01-CA-137894, R01-CA-171979, R01-CA-177423 and P01-CA-174439","R01 CA171979"],"pubmed_authors":["Singh RK","El-Naccache DW","Jha HC","Upadhyay SK","Sahu SK","Robertson ES","Sun Z"],"additional_accession":[]},"is_claimable":false,"name":"KSHV-Mediated Regulation of Par3 and SNAIL Contributes to B-Cell Proliferation.","description":"Studies have suggested that Epithelial-Mesenchymal Transition (EMT) and transformation is an important step in progression to cancer. Par3 (partitioning-defective protein) is a crucial factor in regulating epithelial cell polarity. However, the mechanism by which the latency associated nuclear antigen (LANA) encoded by Kaposi's Sarcoma associated herpesvirus (KSHV) regulates Par3 and EMTs markers (Epithelial-Mesenchymal Transition) during viral-mediated B-cell oncogenesis has not been fully explored. Moreover, several studies have demonstrated a crucial role for EMT markers during B-cell malignancies. In this study, we demonstrate that Par3 is significantly up-regulated in KSHV-infected primary B-cells. Further, Par3 interacted with LANA in KSHV positive and LANA expressing cells which led","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jul","modification":"2025-04-25T22:28:13.92Z","creation":"2019-03-26T22:47:58Z"},"accession":"S-EPMC4963126","cross_references":{"pubmed":["27463802"],"doi":["10.1371/journal.ppat.1005801"]}}