{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Arakaki AKS"],"funding":["Howard Hughes Medical Institute","NCI NIH HHS","National Institutes of Health","NIGMS NIH HHS"],"pagination":["jcs254888"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8084569"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(8)"],"pubmed_abstract":["The α-arrestin domain containing protein 3 (ARRDC3) is a tumor suppressor in triple-negative breast carcinoma (TNBC), a highly metastatic subtype of breast cancer that lacks targeted therapies. Thus, understanding the mechanisms and targets of ARRDC3 in TNBC is important. ARRDC3 regulates trafficking of protease-activated receptor 1 (PAR1, also known as F2R), a G-protein-coupled receptor (GPCR) implicated in breast cancer metastasis. Loss of ARRDC3 causes overexpression of PAR1 and aberrant signaling. Moreover, dysregulation of GPCR-induced Hippo signaling is associated with breast cancer progression. However, the mechanisms responsible for Hippo dysregulation remain unknown. Here, we report that the Hippo pathway transcriptional co-activator TAZ (also known as WWTR1) is the major effector"],"journal":["Journal of cell science"],"pubmed_title":["α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis."],"pmcid":["PMC8084569"],"funding_grant_id":["T32 CA080416","R35 GM127121"],"pubmed_authors":["Pan WA","Wedegaertner H","Trejo J","Chinn L","Arakaki AKS","Gujral TS","Roca-Mercado I"],"additional_accession":[]},"is_claimable":false,"name":"α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis.","description":"The α-arrestin domain containing protein 3 (ARRDC3) is a tumor suppressor in triple-negative breast carcinoma (TNBC), a highly metastatic subtype of breast cancer that lacks targeted therapies. Thus, understanding the mechanisms and targets of ARRDC3 in TNBC is important. ARRDC3 regulates trafficking of protease-activated receptor 1 (PAR1, also known as F2R), a G-protein-coupled receptor (GPCR) implicated in breast cancer metastasis. Loss of ARRDC3 causes overexpression of PAR1 and aberrant signaling. Moreover, dysregulation of GPCR-induced Hippo signaling is associated with breast cancer progression. However, the mechanisms responsible for Hippo dysregulation remain unknown. Here, we report that the Hippo pathway transcriptional co-activator TAZ (also known as WWTR1) is the major effector","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-03-18T13:18:24.022Z","creation":"2025-04-04T10:15:44.088Z"},"accession":"S-EPMC8084569","cross_references":{"pubmed":["33722977"],"doi":["10.1242/jcs.254888"]}}