دورية أكاديمية
أعرض في EDS

Regulation of Orai1/STIM1 mediated I CRAC by intracellular pH.

التفاصيل البيبلوغرافية
العنوان: Regulation of Orai1/STIM1 mediated I CRAC by intracellular pH.
المؤلفون: Gavriliouk D; School of Medical Sciences, University of Adelaide, Adelaide, South Australia, 5005, Australia., Scrimgeour NR; School of Medical Sciences, University of Adelaide, Adelaide, South Australia, 5005, Australia., Grigoryev S; School of Medicine, University of Adelaide, and South Australian Health and Medical Research Institute, Adelaide, South Australia, 5005, Australia., Ma L; School of Medical Sciences, University of Adelaide, Adelaide, South Australia, 5005, Australia.; Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia., Zhou FH; School of Medicine, University of Adelaide, and South Australian Health and Medical Research Institute, Adelaide, South Australia, 5005, Australia., Barritt GJ; School of Medicine, Flinders University of South Australia, Bedford Park, South Australia, 5065, Australia., Rychkov GY; School of Medical Sciences, University of Adelaide, Adelaide, South Australia, 5005, Australia. Grigori.Rychkov@adelaide.edu.au.; School of Medicine, University of Adelaide, and South Australian Health and Medical Research Institute, Adelaide, South Australia, 5005, Australia. Grigori.Rychkov@adelaide.edu.au.
المصدر: Scientific reports [Sci Rep] 2017 Aug 29; Vol. 7 (1), pp. 9829. Date of Electronic Publication: 2017 Aug 29.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Gene Expression Regulation* , Hydrogen-Ion Concentration*, Calcium Release Activated Calcium Channels/*metabolism , Neoplasm Proteins/*genetics , ORAI1 Protein/*genetics , Stromal Interaction Molecule 1/*genetics, Calcium/metabolism ; Cell Line ; Humans ; Intracellular Space/metabolism ; Ion Channel Gating ; Mutation ; Neoplasm Proteins/metabolism ; ORAI1 Protein/metabolism ; Stromal Interaction Molecule 1/metabolism
مستخلص: Ca 2+ release activated Ca 2+ (CRAC) channels composed of two cellular proteins, Ca 2+ -sensing stromal interaction molecule 1 (STIM1) and pore-forming Orai1, are the main mediators of the Ca 2+ entry pathway activated in response to depletion of intracellular Ca 2+ stores. Previously it has been shown that the amplitude of CRAC current (I CRAC ) strongly depends on extracellular and intracellular pH. Here we investigate the intracellular pH (pH i ) dependence of I CRAC mediated by Orai1 and STIM1ectopically expressed in HEK293 cells. The results indicate that pH i affects not only the amplitude of the current, but also Ca 2+ dependent gating of CRAC channels. Intracellular acidification changes the kinetics of I CRAC , introducing prominent re-activation component in the currents recorded in response to voltage steps to strongly negative potentials. I CRAC with similar kinetics can be observed at normal pH i if the expression levels of Orai1 are increased, relative to the expression levels of STIM1. Mutations in the STIM1 inactivation domain significantly diminish the dependence of I CRAC kinetics on pH i , but have no effect on pH i dependence of I CRAC amplitude, implying that more than one mechanism is involved in CRAC channel regulation by intracellular pH.
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المشرفين على المادة: 0 (Calcium Release Activated Calcium Channels)
0 (Neoplasm Proteins)
0 (ORAI1 Protein)
0 (ORAI1 protein, human)
0 (STIM1 protein, human)
0 (Stromal Interaction Molecule 1)
SY7Q814VUP (Calcium)
تواريخ الأحداث: Date Created: 20170831 Date Completed: 20190423 Latest Revision: 20190423
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC5575016
DOI: 10.1038/s41598-017-06371-0
PMID: 28851859
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/s41598-017-06371-0