{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["110(7)"],"submitter":["Juhl OJ"],"funding":["Virginia Commonwealth University Alice T. and William H. Goodwin, Jr. Endowment"],"pubmed_abstract":["The mechanism by which substrate surface characteristics are transduced by osteoblastic cells and their progenitors is not fully known. Data from previous studies by our group suggest the involvement of β-catenin in the mechanism by which substrate surface characteristics are transduced. This focal adhesion and β-catenin mediated mechanism functions through the liberation of β-catenin from focal adhesion complexes in response to pro-osteogenic substrate (POS) characteristics. After liberation, β-catenin translocates and facilitates upregulation of genes associated with osteogenesis. It is not known whether the observed correlation between focal adhesion turnover and β-catenin translocation directly results from focal adhesion turnover. In this study we inhibited focal adhesion turnover using a focal adhesion kinase inhibitor PF-573228. We found that inhibition of focal adhesion turnover resulted in an abrogation of the more rapid translocation and increased transcriptional activity of β-catenin induced by POS. In addition, inhibition of focal adhesion turnover mitigated the increase in osteoblastic differentiation induced by a POS as measured by alkaline phosphatase enzymatic activity and osteogenic gene and protein expression. Together, these data, coupled with previous findings, suggest that the observed β-catenin translocation is a result of focal adhesion turnover, providing evidence for a focal adhesion initiated, β-catenin mediated mechanism of substrate surface signal transduction."],"journal":["Journal of biomedical materials research. Part B, Applied biomaterials"],"pagination":["1573-1586"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9306686"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of focal adhesion turnover prevents osteoblastic differentiation through β-catenin mediated transduction of pro-osteogenic substrate."],"pmcid":["PMC9306686"],"pubmed_authors":["Juhl OJ","Zhang Y","Merife AB","Donahue HJ"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of focal adhesion turnover prevents osteoblastic differentiation through β-catenin mediated transduction of pro-osteogenic substrate.","description":"The mechanism by which substrate surface characteristics are transduced by osteoblastic cells and their progenitors is not fully known. Data from previous studies by our group suggest the involvement of β-catenin in the mechanism by which substrate surface characteristics are transduced. This focal adhesion and β-catenin mediated mechanism functions through the liberation of β-catenin from focal adhesion complexes in response to pro-osteogenic substrate (POS) characteristics. After liberation, β-catenin translocates and facilitates upregulation of genes associated with osteogenesis. It is not known whether the observed correlation between focal adhesion turnover and β-catenin translocation directly results from focal adhesion turnover. In this study we inhibited focal adhesion turnover using a focal adhesion kinase inhibitor PF-573228. We found that inhibition of focal adhesion turnover resulted in an abrogation of the more rapid translocation and increased transcriptional activity of β-catenin induced by POS. In addition, inhibition of focal adhesion turnover mitigated the increase in osteoblastic differentiation induced by a POS as measured by alkaline phosphatase enzymatic activity and osteogenic gene and protein expression. Together, these data, coupled with previous findings, suggest that the observed β-catenin translocation is a result of focal adhesion turnover, providing evidence for a focal adhesion initiated, β-catenin mediated mechanism of substrate surface signal transduction.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2024-11-09T15:46:45.274Z","creation":"2022-08-03T07:10:07.186Z"},"accession":"S-EPMC9306686","cross_references":{"pubmed":["35099117"],"doi":["10.1002/jbm.b.35018"]}}