<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Konietzny A</submitter><funding>Gemeinnützige Hertie-Stiftung</funding><funding>European Research Council</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>Alexander von Humboldt-Stiftung</funding><pagination>e106523</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8844991</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(4)</volume><pubmed_abstract>Excitatory synapses of principal hippocampal neurons are frequently located on dendritic spines. The dynamic strengthening or weakening of individual inputs results in structural and molecular diversity of dendritic spines. Active spines with large calcium ion (Ca&lt;sup>2+&lt;/sup> ) transients are frequently invaded by a single protrusion from the endoplasmic reticulum (ER), which is dynamically transported into spines via the actin-based motor myosin V. An increase in synaptic strength correlates with stable anchoring of the ER, followed by the formation of an organelle referred to as the spine apparatus. Here, we show that myosin V binds the Ca&lt;sup>2+&lt;/sup> sensor caldendrin, a brain-specific homolog of the well-known myosin V interactor calmodulin. While calmodulin is an essential activator</pubmed_abstract><journal>The EMBO journal</journal><pubmed_title>Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines.</pubmed_title><pmcid>PMC8844991</pmcid><funding_grant_id>EXC‐2049‐390688087</funding_grant_id><funding_grant_id>FOR2419 TP2</funding_grant_id><funding_grant_id>759661</funding_grant_id><funding_grant_id>StG‐2017 759661</funding_grant_id><funding_grant_id>MI1923/1‐2</funding_grant_id><funding_grant_id>SFB877 B12</funding_grant_id><pubmed_authors>Demmers JAA</pubmed_authors><pubmed_authors>Mikhaylova M</pubmed_authors><pubmed_authors>Uetrecht C</pubmed_authors><pubmed_authors>Konietzny A</pubmed_authors><pubmed_authors>Hertrich N</pubmed_authors><pubmed_authors>Grunewald K</pubmed_authors><pubmed_authors>Grendel J</pubmed_authors><pubmed_authors>Han Y</pubmed_authors><pubmed_authors>Dekkers DHW</pubmed_authors><pubmed_authors>Bucher M</pubmed_authors><pubmed_authors>Kadek A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines.</name><description>Excitatory synapses of principal hippocampal neurons are frequently located on dendritic spines. The dynamic strengthening or weakening of individual inputs results in structural and molecular diversity of dendritic spines. Active spines with large calcium ion (Ca&lt;sup>2+&lt;/sup> ) transients are frequently invaded by a single protrusion from the endoplasmic reticulum (ER), which is dynamically transported into spines via the actin-based motor myosin V. An increase in synaptic strength correlates with stable anchoring of the ER, followed by the formation of an organelle referred to as the spine apparatus. Here, we show that myosin V binds the Ca&lt;sup>2+&lt;/sup> sensor caldendrin, a brain-specific homolog of the well-known myosin V interactor calmodulin. While calmodulin is an essential activator</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2026-03-27T16:43:30.941Z</modification><creation>2025-02-19T03:58:51.006Z</creation></dates><accession>S-EPMC8844991</accession><cross_references><pubmed>34935159</pubmed><doi>10.15252/embj.2020106523</doi></cross_references></HashMap>