{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen B"],"funding":["NCRR NIH HHS","NIDDK NIH HHS","NCI NIH HHS"],"pagination":["686-93"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4990496"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(9)"],"pubmed_abstract":["Scribble (SCRIB) is a tumor-suppressor protein, playing critical roles in establishing and maintaining epithelial cell polarity. SCRIB is frequently amplified in human cancers but does not localize properly to cell-cell junctions, suggesting that mislocalization of SCRIB disrupts its tumor-suppressive activities. Using chemical reporters, here we showed that SCRIB localization was regulated by S-palmitoylation at conserved cysteine residues. Palmitoylation-deficient mutants of SCRIB were mislocalized, leading to disruption of cell polarity and loss of their tumor-suppressive activities to oncogenic YAP, MAPK and PI3K/AKT pathways. We further found that ZDHHC7 was the major palmitoyl acyltransferase regulating SCRIB. Knockout of ZDHHC7 led to SCRIB mislocalization and YAP activation, and di"],"journal":["Nature chemical biology"],"pubmed_title":["ZDHHC7-mediated S-palmitoylation of Scribble regulates cell polarity."],"pmcid":["PMC4990496"],"funding_grant_id":["R01 CA181537","R01 DK107651","S10 RR027673"],"pubmed_authors":["Brooks YS","Fu J","Zheng B","DeRan M","Chen B","Jarugumilli GK","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"ZDHHC7-mediated S-palmitoylation of Scribble regulates cell polarity.","description":"Scribble (SCRIB) is a tumor-suppressor protein, playing critical roles in establishing and maintaining epithelial cell polarity. SCRIB is frequently amplified in human cancers but does not localize properly to cell-cell junctions, suggesting that mislocalization of SCRIB disrupts its tumor-suppressive activities. Using chemical reporters, here we showed that SCRIB localization was regulated by S-palmitoylation at conserved cysteine residues. Palmitoylation-deficient mutants of SCRIB were mislocalized, leading to disruption of cell polarity and loss of their tumor-suppressive activities to oncogenic YAP, MAPK and PI3K/AKT pathways. We further found that ZDHHC7 was the major palmitoyl acyltransferase regulating SCRIB. Knockout of ZDHHC7 led to SCRIB mislocalization and YAP activation, and di","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Sep","modification":"2025-04-21T18:41:10.32Z","creation":"2019-03-27T02:21:00Z"},"accession":"S-EPMC4990496","cross_references":{"pubmed":["27380321"],"doi":["10.1038/nchembio.2119"]}}