<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(1)</volume><submitter>Hatano R</submitter><pubmed_abstract>Ezrin is highly expressed in glomerular podocytes and is reported to form a multi-protein complex with scaffold protein Na+/H+ exchanger regulatory factor 2 (NHERF2) and podocalyxin, a major sialoprotein. Podocalyxin-knockout mice died within 24 h of birth with anuric renal failure, whereas NHERF2-knockout mice show no apparent changes in the glomerular functions. However, the physiological roles of ezrin in glomerular podocytes remain unclear. Here, we investigated the importance of ezrin in the regulation of glomerular podocyte function using ezrin-knockdown mice (Vil2 kd/kd ). The Vil2 kd/kd mice did not exhibit apparent glomerular dysfunction, morphological defects or abnormal localisation of podocalyxin and NHERF2 in podocytes. Thus, we investigated the influence of ezrin defects on R</pubmed_abstract><journal>Scientific reports</journal><pagination>4512</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5852236</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Loss of ezrin expression reduced the susceptibility to the glomerular injury in mice.</pubmed_title><pmcid>PMC5852236</pmcid><pubmed_authors>Kawaguchi K</pubmed_authors><pubmed_authors>Hatano R</pubmed_authors><pubmed_authors>Takeda A</pubmed_authors><pubmed_authors>Kazama I</pubmed_authors><pubmed_authors>Matsubara M</pubmed_authors><pubmed_authors>Abe Y</pubmed_authors><pubmed_authors>Asano S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Loss of ezrin expression reduced the susceptibility to the glomerular injury in mice.</name><description>Ezrin is highly expressed in glomerular podocytes and is reported to form a multi-protein complex with scaffold protein Na+/H+ exchanger regulatory factor 2 (NHERF2) and podocalyxin, a major sialoprotein. Podocalyxin-knockout mice died within 24 h of birth with anuric renal failure, whereas NHERF2-knockout mice show no apparent changes in the glomerular functions. However, the physiological roles of ezrin in glomerular podocytes remain unclear. Here, we investigated the importance of ezrin in the regulation of glomerular podocyte function using ezrin-knockdown mice (Vil2 kd/kd ). The Vil2 kd/kd mice did not exhibit apparent glomerular dysfunction, morphological defects or abnormal localisation of podocalyxin and NHERF2 in podocytes. Thus, we investigated the influence of ezrin defects on R</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Mar</publication><modification>2025-04-04T09:05:05.579Z</modification><creation>2019-03-26T23:23:03Z</creation></dates><accession>S-EPMC5852236</accession><cross_references><pubmed>29540766</pubmed><doi>10.1038/s41598-018-22846-0</doi></cross_references></HashMap>