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http://purl.uniprot.org/citations/31018906http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31018906http://www.w3.org/2000/01/rdf-schema#comment"Store-operated calcium entry (SOCE) modulates cytosolic calcium in multiple cells. Endoplasmic reticulum (ER)-localized STIM1 and plasma membrane (PM)-localized ORAI1 are two main components of SOCE. STIM1:ORAI1 association requires STIM1 oligomerization, its re-distribution to ER-PM junctions, and puncta formation. However, little is known about the negative regulation of these steps to prevent calcium overload. Here, we identified Tmem178 as a negative modulator of STIM1 puncta formation in myeloid cells. Using site-directed mutagenesis, co-immunoprecipitation assays and FRET imaging, we determined that Tmem178:STIM1 association occurs via their transmembrane motifs. Mutants that increase Tmem178:STIM1 association reduce STIM1 puncta formation, SOCE activation, impair inflammatory cytokine production in macrophages and osteoclastogenesis. Mutants that reduce Tmem178:STIM1 association reverse these effects. Furthermore, exposure to plasma from arthritic patients decreases Tmem178 expression, enhances SOCE activation and cytoplasmic calcium. In conclusion, Tmem178 modulates the rate-limiting step of STIM1 puncta formation and therefore controls SOCE in inflammatory conditions."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.org/dc/terms/identifier"doi:10.1016/j.jaut.2019.04.015"xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Yang Z."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Zhou Y."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Yan H."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Jing J."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Dai W."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Mahajan S."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Faccio R."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Mellins E.D."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Macaubas C."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Fitzpatrick J.A.J."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/author"Shih C.C."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/name"J Autoimmun"xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/pages"94-108"xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/title"Tmem178 negatively regulates store-operated calcium entry in myeloid cells via association with STIM1."xsd:string
http://purl.uniprot.org/citations/31018906http://purl.uniprot.org/core/volume"101"xsd:string
http://purl.uniprot.org/citations/31018906http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31018906
http://purl.uniprot.org/citations/31018906http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31018906
http://purl.uniprot.org/uniprot/#_G0XQ39-mappedCitation-31018906http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31018906
http://purl.uniprot.org/uniprot/#_H3BS89-mappedCitation-31018906http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31018906