IndraLab

Statements


USP5 deubiquitinates CACNA1H. 4 / 5
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"As reported, overexpression of USP5 decreases ubiquitination of CaV3.2, which in turn decreases channel internalization [64]."

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"Thus, targeting Cav3.2 deubiquitination by USP5 is a potential therapeutic target for pain associated with inflammatory disorders [62]."

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"Knockdown of USP5 via shRNA increases Cav3.2 ubiquitination, decreases Cav3.2 protein levels, and reduces Cav3.2 whole-cell currents."

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"Deubiquitination of Cav3.2 by USP5 promotes channel stability and function, thus mediating the development of neuropathic and inflammatory pain in rodents [7]."