HDAC10 switches NLRP3 modification from acetylation to ubiquitination and attenuates acute inflammatory diseases

HDAC10 switches NLRP3 modification from acetylation to ubiquitination and attenuates acute inflammatory diseases

Abstract Background The NOD-like receptor protein (NLRP)3 inflammasome is at the signaling hub center to instigate inflammation in response to pathogen infection or oxidative stress, and its tight control is pivotal for immune defense against infection while avoiding parallel intensive inflammatory...

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Bibliographic Details
Main Authors: Min Yang, Zhenzhi Qin, Yueke Lin, Dapeng Ma, Caiyu Sun, Haocheng Xuan, Xiuling Cui, Wei Ma, Xinyi Zhu, Lihui Han
Format: Article
Language:English
Published: BMC 2024-12-01
Series:Cell Communication and Signaling
Subjects:
HDAC10
NLRP3 inflammasome
Deacetylation
Ubiquitination
Acute inflammation
Online Access:https://doi.org/10.1186/s12964-024-01992-1
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https://doi.org/10.1186/s12964-024-01992-1

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