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The purpose of the present study was to investigate its effects on T\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels. Using patch\u2010clamp electrophysiology, we demonstrate that the H\n                    <jats:sub>2<\/jats:sub>\n                    S donor, NaHS (10 \u03bcM\u20131 mM) selectively inhibits Cav3.2 T\u2010type channels heterologously expressed in HEK293 cells, whereas Cav3.1 and Cav3.3 channels were unaffected. The sensitivity of Cav3.2 channels to H\n                    <jats:sub>2<\/jats:sub>\n                    S required the presence of the redox\u2010sensitive extracellular residue H191, which is also required for tonic binding of Zn\n                    <jats:sup>2+<\/jats:sup>\n                    to this channel. Chelation of Zn\n                    <jats:sup>2+<\/jats:sup>\n                    with\n                    <jats:italic>N<\/jats:italic>\n                    ,\n                    <jats:italic>N<\/jats:italic>\n                    ,\n                    <jats:italic>N<\/jats:italic>\n                    \u2018,\n                    <jats:italic>N<\/jats:italic>\n                    \u2018\u2010tetra\u20102\u2010picolylethylenediamine prevented channel inhibition by H\n                    <jats:sub>2<\/jats:sub>\n                    S and also reversed H\n                    <jats:sub>2<\/jats:sub>\n                    S inhibition when applied after H\n                    <jats:sub>2<\/jats:sub>\n                    S exposure, suggesting that H\n                    <jats:sub>2<\/jats:sub>\n                    S may act\n                    <jats:italic>via<\/jats:italic>\n                    increasing the affinity of the channel for extracellular Zn\n                    <jats:sup>2+<\/jats:sup>\n                    binding. Inhibition of native T\u2010type channels in 3 cell lines correlated with expression of Cav3.2 and not Cav3.1 channels. Notably, H\n                    <jats:sub>2<\/jats:sub>\n                    S also inhibited native T\u2010type (primarily Cav3.2) channels in sensory dorsal root ganglion neurons. Our data demonstrate a novel target for H\n                    <jats:sub>2<\/jats:sub>\n                    S regulation, the T\u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel Cav3.2, and suggest that such modulation cannot account for the pronociceptive effects of this gasotransmitter.\u2014Elies, J., Scragg, J. L., Huang, S., Dallas, M. L., Huang, D., MacDougall, D., Boyle, J. P., Gamper, N., Peers, C., Hydrogen sulfide inhibits Cav3.2 T\u2010type Ca2+ channels. FASEB J. 28, 5376\u20135387 (2014).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.14-257113","type":"journal-article","created":{"date-parts":[[2014,9,3]],"date-time":"2014-09-03T01:45:29Z","timestamp":1409708729000},"page":"5376-5387","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Hydrogen sulfide inhibits Cav3.2 T\u2010type Ca\n                    <sup>2+<\/sup>\n                    channels"],"prefix":"10.1096","volume":"28","author":[{"given":"Jacobo","family":"Elies","sequence":"first","affiliation":[{"name":"Division of Cardiovascular and Diabetes Research Leeds Institute of Cardiovascular and Metabolic Medicine Faculty of Medicine and Health University of Leeds Leeds UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jason L.","family":"Scragg","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular and Diabetes Research Leeds Institute of Cardiovascular and Metabolic Medicine Faculty of Medicine and Health University of Leeds Leeds UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sha","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark L.","family":"Dallas","sequence":"additional","affiliation":[{"name":"School of Pharmacy University of Reading Reading UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongyang","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"MacDougall","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences Faculty of Biological Sciences University of Leeds Leeds UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John P.","family":"Boyle","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular and Diabetes Research Leeds Institute of Cardiovascular and Metabolic Medicine Faculty of Medicine and Health University of Leeds Leeds UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nikita","family":"Gamper","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences Faculty of Biological Sciences University of Leeds Leeds UK"},{"name":"Department of Pharmacology Hebei Medical University Shijiazhuang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chris","family":"Peers","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular and Diabetes Research Leeds Institute of Cardiovascular and Metabolic Medicine Faculty of Medicine and Health University of Leeds Leeds 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