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Statements

USP5 activates CACNA1H. 11 / 11
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"If so, our data suggest that this function involves a USP5-mediated upregulation of Cav3.2 channel activity in the afferent pain pathway."
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"Interestingly, chronic injury models also induce a USP5-mediated enhancement of Cav3.2 channels in the DRG and spinal cord ( García-Caballero et al., 2014 )."
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"CaV3.2 can be upregulated by increased expression of USP5 , which interacts with and de-ubiquitinates these channels thereby decreasing their degradation ( Garcia-Caballero et al ., 2014 ; Stemkowski et al ., 2016 ) ."
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"In the present study, we test the hypothesis that IL-1β activity can trigger USP5-mediated Cav3.2 channel plasticity to induce pain."
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"The deubiquitinating enzyme USP5 modulates neuropathic and inflammatory pain by enhancing Cav3.2 channel activity."
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"On the contrary, knockdown of USP5 reduced Cav3.2 currents in Cath.a-differentiated (CAD) cells, which express USP5 endogenously."
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"USP5 is aberrantly upregulated, and the UBP domain of USP5 can interact with the III-IV linker of the Cav3.2 T-type channel, enhancing Cav3.2 stability and whole-cell current under various painful con[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Furthermore, no sex difference exists in the USP5-mediated dysregulation of Cav3.2 [ 56 ]."
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"We propose that USP5 modulation of Cav3.2 channels enhances sensory modality of nociceptors whose primary physiological function may be to trigger a protective pain state after injury.Transient recept[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"USP5 interacts with and modulates the activity of Cav3.2 calcium channel, yet its binding capacity is impaired by SUMO2/3 modification45."
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"Importantly, USP5 is upregulated during various chronic pain conditions, thereby increasing Cav3.2 channel stability in the PM due to reduced ubiquitination of the channels."
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