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"When the nerve is damaged , USP5 enhances the deubiquitination of the Cav3.2 channel in the dorsal horn , increasing T-type calcium current , which in turn causes pain hypersensitivity ( Gadotti et al ., 2015 ; Gadotti and Zamponi , 2018 ; Ozaki et al ., 2018 ) ."

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"It is also particularly interesting that BCA, the reversible inhibitor of CSE, prevented the upregulation of Ca v 3.2, Egr-1 and USP5 (see Fig. 9 ), in addition to the bladder pain/referred hyperalges[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"This would add to the already elevated level of USP5, which would enhance the deubiquitinylation of Ca 3.2 and further potentiate the expression of the channel in the plasma membrane.Asparagine (N)-linked glycosylation is another type of post-translational modification that has been reported to potentially contribute to peripheral painful diabetic neuropathy."