<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Karunakaran U</submitter><funding>KNU</funding><funding>NRF</funding><funding>National Research Foundation of Korea</funding><funding>Kyungpook National University</funding><pagination>192-205</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6470101</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(2)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Chronic hyperglycemia has deleterious effects on pancreatic β-cell function and turnover. Recent studies support the view that cyclin-dependent kinase 5 (CDK5) plays a role in β-cell failure under hyperglycemic conditions. However, little is known about how CDK5 impair β-cell function. Myricetin, a natural flavonoid, has therapeutic potential for the treatment of type 2 diabetes mellitus. In this study, we examined the effect of myricetin on high glucose (HG)-induced β-cell apoptosis and explored the relationship between myricetin and CDK5.&lt;h4>Methods&lt;/h4>To address this question, we subjected INS-1 cells and isolated rat islets to HG conditions (30 mM) in the presence or absence of myricetin. Docking studies were conducted to validate the interaction between myricetin a</pubmed_abstract><journal>Diabetes &amp; metabolism journal</journal><pubmed_title>Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5.</pubmed_title><pmcid>PMC6470101</pmcid><funding_grant_id>2016R1E1A2020567</funding_grant_id><pubmed_authors>Moon JS</pubmed_authors><pubmed_authors>Jeon JH</pubmed_authors><pubmed_authors>Kim ND</pubmed_authors><pubmed_authors>Park KG</pubmed_authors><pubmed_authors>Leem J</pubmed_authors><pubmed_authors>Elumalai S</pubmed_authors><pubmed_authors>Won KC</pubmed_authors><pubmed_authors>Karunakaran U</pubmed_authors><pubmed_authors>Lee IK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5.</name><description>&lt;h4>Background&lt;/h4>Chronic hyperglycemia has deleterious effects on pancreatic β-cell function and turnover. Recent studies support the view that cyclin-dependent kinase 5 (CDK5) plays a role in β-cell failure under hyperglycemic conditions. However, little is known about how CDK5 impair β-cell function. Myricetin, a natural flavonoid, has therapeutic potential for the treatment of type 2 diabetes mellitus. In this study, we examined the effect of myricetin on high glucose (HG)-induced β-cell apoptosis and explored the relationship between myricetin and CDK5.&lt;h4>Methods&lt;/h4>To address this question, we subjected INS-1 cells and isolated rat islets to HG conditions (30 mM) in the presence or absence of myricetin. Docking studies were conducted to validate the interaction between myricetin a</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Apr</publication><modification>2026-07-17T01:36:08.078Z</modification><creation>2019-06-06T22:56:58Z</creation></dates><accession>S-EPMC6470101</accession><cross_references><pubmed>30688049</pubmed><doi>10.4093/dmj.2018.0052</doi></cross_references></HashMap>