<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Arige V</submitter><funding>NIDCR NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>jcs258875</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8601716</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>134(20)</volume><pubmed_abstract>Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) play a central role in regulating intracellular Ca2+ signals in response to a variety of internal and external cues. Dysregulation of IP3R signaling is the underlying cause for numerous pathological conditions. It is well established that the activities of IP3Rs are governed by several post-translational modifications, including phosphorylation by protein kinase A (PKA). However, the long-term effects of PKA activation on expression of IP3R subtypes remains largely unexplored. In this report, we investigate the effects of chronic stimulation and tonic activity of PKA on the expression of IP3R subtypes. We demonstrate that expression of the type 1 IP3R (IP3R1) is augmented upon prolonged activation of PKA or upon ectopic overexpression of</pubmed_abstract><journal>Journal of cell science</journal><pubmed_title>CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.</pubmed_title><pmcid>PMC8601716</pmcid><funding_grant_id>R01 DE014756</funding_grant_id><pubmed_authors>Yule DI</pubmed_authors><pubmed_authors>Malik S</pubmed_authors><pubmed_authors>Arige V</pubmed_authors><pubmed_authors>Knebel TR</pubmed_authors><pubmed_authors>Terry LE</pubmed_authors><pubmed_authors>Wagner Ii LE</pubmed_authors></additional><is_claimable>false</is_claimable><name>CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.</name><description>Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) play a central role in regulating intracellular Ca2+ signals in response to a variety of internal and external cues. Dysregulation of IP3R signaling is the underlying cause for numerous pathological conditions. It is well established that the activities of IP3Rs are governed by several post-translational modifications, including phosphorylation by protein kinase A (PKA). However, the long-term effects of PKA activation on expression of IP3R subtypes remains largely unexplored. In this report, we investigate the effects of chronic stimulation and tonic activity of PKA on the expression of IP3R subtypes. We demonstrate that expression of the type 1 IP3R (IP3R1) is augmented upon prolonged activation of PKA or upon ectopic overexpression of</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-06-18T07:47:24.765Z</modification><creation>2025-04-05T18:14:34.622Z</creation></dates><accession>S-EPMC8601716</accession><cross_references><pubmed>34533188</pubmed><doi>10.1242/jcs.258875</doi></cross_references></HashMap>