{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hogea A"],"funding":["Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["2103-2123"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7618066"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["599(7)"],"pubmed_abstract":["<h4>Key points</h4>Rat somatosensory neurons express a junctional protein, junctophilin-4 (JPH4) JPH4 is necessary for the formation of store operated Ca<sup>2+</sup> entry (SOCE) complex at the junctions between plasma membrane and endoplasmic reticulum in these neurons. Knockdown of JPH4 impairs endoplasmic reticulum Ca<sup>2+</sup> store refill and junctional Ca<sup>2+</sup> signalling in sensory neurons. In vivo knockdown of JPH4 in the dorsal root ganglion (DRG) sensory neurons significantly attenuated experimentally induced inflammatory pain in rats. Junctional nanodomain Ca<sup>2+</sup> signalling maintained by JPH4 is an important contributor to the inflammatory pain mechanisms.<h4>Abstract</h4>Junctions of endoplasmic reticulum and plasma membrane (ER-PM junctions) form signalling"],"journal":["The Journal of physiology"],"pubmed_title":["Junctophilin-4 facilitates inflammatory signalling at plasma membrane-endoplasmic reticulum junctions in sensory neurons."],"pmcid":["PMC7618066"],"funding_grant_id":["BB/R003068/1","BB/R02104X/1","212302/Z/18/Z","212302"],"pubmed_authors":["Liang C","Gamper N","Huang D","Shah S","Hogea A","Jones F","Du X","Hao H","Carver CM"],"additional_accession":[]},"is_claimable":false,"name":"Junctophilin-4 facilitates inflammatory signalling at plasma membrane-endoplasmic reticulum junctions in sensory neurons.","description":"<h4>Key points</h4>Rat somatosensory neurons express a junctional protein, junctophilin-4 (JPH4) JPH4 is necessary for the formation of store operated Ca<sup>2+</sup> entry (SOCE) complex at the junctions between plasma membrane and endoplasmic reticulum in these neurons. Knockdown of JPH4 impairs endoplasmic reticulum Ca<sup>2+</sup> store refill and junctional Ca<sup>2+</sup> signalling in sensory neurons. In vivo knockdown of JPH4 in the dorsal root ganglion (DRG) sensory neurons significantly attenuated experimentally induced inflammatory pain in rats. Junctional nanodomain Ca<sup>2+</sup> signalling maintained by JPH4 is an important contributor to the inflammatory pain mechanisms.<h4>Abstract</h4>Junctions of endoplasmic reticulum and plasma membrane (ER-PM junctions) form signalling","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-05-18T03:09:20.776Z","creation":"2026-05-18T03:07:13.805Z"},"accession":"S-EPMC7618066","cross_references":{"pubmed":["33569781"],"doi":["10.1113/JP281331"]}}