Cdyl Deficiency Brakes Neuronal Excitability and Nociception through Promoting Kcnb1 Transcription in Peripheral Sensory Neurons.
Kv2.1 channel
chromodomain Y-like
epigenetic regulation
novel chromodomain Y-like antagonist
pain sensation
Journal
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
ISSN: 2198-3844
Titre abrégé: Adv Sci (Weinh)
Pays: Germany
ID NLM: 101664569
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
revised:
28
12
2021
received:
28
09
2021
pubmed:
5
2
2022
medline:
8
4
2022
entrez:
4
2
2022
Statut:
ppublish
Résumé
Epigenetic modifications are involved in the onset, development, and maintenance of pain; however, the precise epigenetic mechanism underlying pain regulation remains elusive. Here it is reported that the epigenetic factor chromodomain Y-like (CDYL) is crucial for pain processing. Selective knockout of CDYL in sensory neurons results in decreased neuronal excitability and nociception. Moreover, CDYL facilitates histone 3 lysine 27 trimethylation (H3K27me3) deposition at the Kcnb1 intron region thus silencing voltage-gated potassium channel (K
Identifiants
pubmed: 35119221
doi: 10.1002/advs.202104317
pmc: PMC8981457
doi:
Substances chimiques
Co-Repressor Proteins
0
Histones
0
Kcnb1 protein, mouse
0
Shab Potassium Channels
0
Cdyl protein, mouse
EC 4.2.1.-
Hydro-Lyases
EC 4.2.1.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2104317Subventions
Organisme : NCI NIH HHS
ID : P30 CA016086
Pays : United States
Organisme : NIDA NIH HHS
ID : R61 DA047023
Pays : United States
Organisme : NIDA NIH HHS
ID : R61DA047023-01
Pays : United States
Commentaires et corrections
Type : ErratumIn
Informations de copyright
© 2022 The Authors. Advanced Science published by Wiley-VCH GmbH.
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