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dc.contributor.authorKim, Hyesu-
dc.contributor.authorKim, Hyungsup-
dc.contributor.authorCho, Hawon-
dc.contributor.authorLee, Byeongjun-
dc.contributor.authorLu, Huan-Jun-
dc.contributor.authorKim, Kyungmin-
dc.contributor.authorChung, Sooyoung-
dc.contributor.authorShim, Won-Sik-
dc.contributor.authorShin, Young Kee-
dc.contributor.authorDong, Xinzhong-
dc.contributor.authorWood, John N.-
dc.contributor.authorOh, Uhtaek-
dc.date.accessioned2024-01-19T11:00:22Z-
dc.date.available2024-01-19T11:00:22Z-
dc.date.created2022-11-04-
dc.date.issued2022-11-
dc.identifier.issn0304-3959-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/114409-
dc.description.abstractItch is an unpleasant sensation that evokes a desire to scratch. Pathologic conditions such as allergy or atopic dermatitis produce severe itching sensation. Mas-related G protein receptors (Mrgprs) are receptors for many endogenous pruritogens. However, signaling pathways downstream to these receptors in dorsal root ganglion (DRG) neurons are not yet understood. We found that anoctamin 1 (ANO1), a Ca2+-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of Ano1 in DRG neurons displayed a significant reduction in scratching behaviors in response to acute and chronic Mrgpr-dependent itch models and the epidermal hyperplasia induced by dry skin. In vivo Ca2+ imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of Ano1 in DRG neurons of Ano1-deficient mice rescued the impaired itching observed in Ano1-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.-
dc.languageEnglish-
dc.publisherElsevier BV-
dc.titleAnoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor-dependent itch-
dc.typeArticle-
dc.identifier.doi10.1097/j.pain.0000000000002611-
dc.description.journalClass1-
dc.identifier.bibliographicCitationPain, v.163, no.11, pp.2172 - 2184-
dc.citation.titlePain-
dc.citation.volume163-
dc.citation.number11-
dc.citation.startPage2172-
dc.citation.endPage2184-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000868828900014-
dc.relation.journalWebOfScienceCategoryAnesthesiology-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaAnesthesiology-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeArticle-
dc.subject.keywordPlusBEHAVIORAL-RESPONSES-
dc.subject.keywordPlusSENSORY NEURONS-
dc.subject.keywordPlusMOUSE MODEL-
dc.subject.keywordPlusDRY SKIN-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusHISTAMINE-
dc.subject.keywordPlusPAIN-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusPRURITUS-
dc.subject.keywordPlusPEPTIDE-
dc.subject.keywordAuthorAnoctamin 1-
dc.subject.keywordAuthorPruriceptors-
dc.subject.keywordAuthorItch-
dc.subject.keywordAuthorMrgprs-
dc.subject.keywordAuthorBilirubin-
dc.subject.keywordAuthorChloroquine-
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KIST Article > 2022
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