<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Stickel KC</submitter><funding>NCATS NIH HHS</funding><funding>NEI NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><pubmed_abstract>&lt;h4>Objective&lt;/h4>Spinophilin is an F-actin binding and protein phosphatase 1 (PP1) targeting protein that acts as a scaffold of PP1 to its substrates. Spinophilin knockout (Spino&lt;sup>-/-&lt;/sup>) mice have decreased fat mass, increased lean mass, and improved glucose tolerance, with no difference in feeding behaviors. While spinophilin is enriched in neurons, its roles in non-neuronal tissues, such as beta cells of the pancreatic islets, are unclear.&lt;h4>Methods &amp; results&lt;/h4>We have corroborated and expanded upon previous studies to determine that Spino&lt;sup>-/-&lt;/sup> mice have decreased weight gain and improved glucose tolerance in two different models of obesity. Using proteomics and immunoblotting-based approaches we identified multiple putative spinophilin interacting proteins isolated f</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.02.07.527495</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9934546</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Mechanisms of spinophilin-dependent pancreas dysregulation underlying diabesity.</pubmed_title><pmcid>PMC9934546</pmcid><funding_grant_id>R33 DA041876</funding_grant_id><funding_grant_id>R15 EY033968</funding_grant_id><funding_grant_id>P30 CA082709</funding_grant_id><funding_grant_id>R21 DA041876</funding_grant_id><funding_grant_id>UL1 TR002529</funding_grant_id><funding_grant_id>P30 DK097512</funding_grant_id><pubmed_authors>Belecky-Adams TL</pubmed_authors><pubmed_authors>Baucum AJ</pubmed_authors><pubmed_authors>Doud EH</pubmed_authors><pubmed_authors>Mosley AL</pubmed_authors><pubmed_authors>Stickel KC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mechanisms of spinophilin-dependent pancreas dysregulation underlying diabesity.</name><description>&lt;h4>Objective&lt;/h4>Spinophilin is an F-actin binding and protein phosphatase 1 (PP1) targeting protein that acts as a scaffold of PP1 to its substrates. Spinophilin knockout (Spino&lt;sup>-/-&lt;/sup>) mice have decreased fat mass, increased lean mass, and improved glucose tolerance, with no difference in feeding behaviors. While spinophilin is enriched in neurons, its roles in non-neuronal tissues, such as beta cells of the pancreatic islets, are unclear.&lt;h4>Methods &amp; results&lt;/h4>We have corroborated and expanded upon previous studies to determine that Spino&lt;sup>-/-&lt;/sup> mice have decreased weight gain and improved glucose tolerance in two different models of obesity. Using proteomics and immunoblotting-based approaches we identified multiple putative spinophilin interacting proteins isolated f</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2025-04-04T11:35:20.936Z</modification><creation>2025-04-04T11:35:20.936Z</creation></dates><accession>S-EPMC9934546</accession><cross_references><pubmed>36798361</pubmed><doi>10.1101/2023.02.07.527495</doi></cross_references></HashMap>