Cargando…
Small organic molecule disruptors of Cav3.2 - USP5 interactions reverse inflammatory and neuropathic pain
BACKGROUND: Cav3.2 channels facilitate nociceptive transmission and are upregulated in DRG neurons in response to nerve injury or peripheral inflammation. We reported that this enhancement of Cav3.2 currents in afferent neurons is mediated by deubiquitination of the channels by the deubiquitinase US...
Autores principales: | Gadotti, Vinicius M, Caballero, Agustin Garcia, Berger, N Daniel, Gladding, Clare M, Chen, Lina, Pfeifer, Tom A, Zamponi, Gerald W |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364099/ https://www.ncbi.nlm.nih.gov/pubmed/25889575 http://dx.doi.org/10.1186/s12990-015-0011-8 |
Ejemplares similares
-
A cell-permeant peptide corresponding to the cUBP domain of USP5 reverses inflammatory and neuropathic pain
por: Garcia-Caballero, Agustin, et al.
Publicado: (2016) -
Disrupting USP5/Cav3.2 interactions protects female mice from mechanical hypersensitivity during peripheral inflammation
por: Gadotti, Vinicius M., et al.
Publicado: (2018) -
Identification of interleukin-1 beta as a key mediator in the upregulation of Cav3.2–USP5 interactions in the pain pathway
por: Stemkowski, Patrick L, et al.
Publicado: (2017) -
The terpenes camphene and alpha-bisabolol inhibit inflammatory and neuropathic pain via Cav3.2 T-type calcium channels
por: Gadotti, Vinicius M., et al.
Publicado: (2021) -
SUMOylation regulates USP5-Cav3.2 calcium channel interactions
por: Garcia-Caballero, Agustin, et al.
Publicado: (2019)