Publications

@article{Kim2024,

title = {Anoctamin 1, a multi-modal player in pain and itch},

author = {Hyungsup Kim and Won-Sik Shim and Uhtaek Oh},

doi = {10.1016/j.ceca.2024.102924},

issn = {0143-4160},

year  = {2024},

date = {2024-11-00},

urldate = {2024-11-00},

journal = {Cell Calcium},

volume = {123},

publisher = {Elsevier BV},

keywords = {Anoctamin 1, Itch, pain},

pubstate = {published},

tppubtype = {article}

}

@article{Kim2022,

title = {Anoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor–dependent itch},

author = {Hyesu Kim and Hyungsup Kim and Hawon Cho and Byeongjun Lee and Huan-Jun Lu and Kyungmin Kim and Sooyoung Chung and Won-Sik Shim and Young Kee Shin and Xinzhong Dong and John N. Wood and Uhtaek Oh},

doi = {10.1097/j.pain.0000000000002611},

issn = {1872-6623},

year  = {2022},

date = {2022-00-00},

urldate = {2022-00-00},

journal = {PAIN},

volume = {163},

number = {11},

pages = {2172--2184},

publisher = {Ovid Technologies (Wolters Kluwer Health)},

abstract = {<jats:title>Abstract</jats:title>

          <jats:p>Itch 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 Ca<jats:sup>2+</jats:sup>-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of <jats:italic toggle="yes">Ano1</jats:italic> 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 Ca<jats:sup>2+</jats:sup> imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of <jats:italic toggle="yes">Ano1</jats:italic> in DRG neurons of <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice rescued the impaired itching observed in <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.</jats:p>},

keywords = {Anoctamin 1, Itch, MrgprA3, MrgprC11},

pubstate = {published},

tppubtype = {article}

}