{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gross P"],"funding":["American Heart Association","British Heart Foundation","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute","NINDS NIH HHS"],"pagination":["92-114"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7790862"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["128(1)"],"pubmed_abstract":["<h4>Rationale</h4>Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release (CICR) in normal hearts requires close approximation of L-type calcium channels (LTCCs) within the transverse tubules (T-tubules) and RyR (ryanodine receptors) within the junctional sarcoplasmic reticulum. CICR is disrupted in cardiac hypertrophy and heart failure, which is associated with loss of T-tubules and disruption of cardiac dyads. In these conditions, LTCCs are redistributed from the T-tubules to disrupt CICR. The molecular mechanism responsible for LTCCs recruitment to and from the T-tubules is not well known. JPH (junctophilin) 2 enables close association between T-tubules and the junctional sarcoplasmic reticulum to ensure efficient CICR. JPH2 has a so-called joining region that is located near domains that inter"],"journal":["Circulation research"],"pubmed_title":["Interaction of the Joining Region in Junctophilin-2 With the L-Type Ca&lt;sup&gt;2+&lt;/sup&gt; Channel Is Pivotal for Cardiac Dyad Assembly and Intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; Dynamics."],"pmcid":["PMC7790862"],"funding_grant_id":["P01 HL147841","RG/17/13/33173","R01 HL147558","T32 HL091804","R01 HL145177","R01 HL139889","16PRE30860001","R01 HL142271","R01 HL136954","RF1 NS121379"],"pubmed_authors":["Garbincius JF","Gross P","Johnson J","Wallner M","Kubo H","Gibb AA","Sabri A","Yu D","Feldsott EA","Sanchez-Alonso J","Lambert J","Romero CM","Lucarelli C","Varol E","Poulet C","Rizzo V","Yang Y","Houser SR","Ross J","Berretta RM","Elrod J","Chen X","Eaton DM","Gorelik J"],"additional_accession":[]},"is_claimable":false,"name":"Interaction of the Joining Region in Junctophilin-2 With the L-Type Ca&lt;sup&gt;2+&lt;/sup&gt; Channel Is Pivotal for Cardiac Dyad Assembly and Intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; Dynamics.","description":"<h4>Rationale</h4>Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release (CICR) in normal hearts requires close approximation of L-type calcium channels (LTCCs) within the transverse tubules (T-tubules) and RyR (ryanodine receptors) within the junctional sarcoplasmic reticulum. CICR is disrupted in cardiac hypertrophy and heart failure, which is associated with loss of T-tubules and disruption of cardiac dyads. In these conditions, LTCCs are redistributed from the T-tubules to disrupt CICR. The molecular mechanism responsible for LTCCs recruitment to and from the T-tubules is not well known. JPH (junctophilin) 2 enables close association between T-tubules and the junctional sarcoplasmic reticulum to ensure efficient CICR. JPH2 has a so-called joining region that is located near domains that inter","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jan","modification":"2025-04-04T00:38:47.757Z","creation":"2022-02-11T14:56:25.758Z"},"accession":"S-EPMC7790862","cross_references":{"pubmed":["33092464"],"doi":["10.1161/circresaha.119.315715","10.1161/CIRCRESAHA.119.315715"]}}