A novel and atypical NF-KB pro-inflammatory program regulated by a CamKII-proteasome axis is involved in the early activation of Muller glia by high glucose

A novel and atypical NF-KB pro-inflammatory program regulated by a CamKII-proteasome axis is involved in the early activation of Muller glia by high glucose

Key Points High glucose quickly induces an atypical NF-kB pro-inflammatory program. CamKII phosphorylation of Rpt6 subunit of the proteasome stimulates IkBα turnover and p65-p50 release. Inhibition of either CamkII or proteasome blocks this pathway.

Bibliographic Details
Main Authors: Diego Sbardella, Grazia Raffaella Tundo, Alice Mecchia, Camilla Palumbo, Maria Grazia Atzori, Lauretta Levati, Alessandra Boccaccini, Anna Maria Caccuri, Paolo Cascio, Pedro Miguel Lacal, Grazia Graziani, Monica Varano, Massimiliano Coletta, Mariacristina Parravano
Format: Article
Language:English
Published: BMC 2022-07-01
Series:Cell & Bioscience
Subjects:
Diabetic retinopathy
Muller glia
NF-kB pathway
Proteasome
CamKII
Online Access:https://doi.org/10.1186/s13578-022-00839-x

Internet

https://doi.org/10.1186/s13578-022-00839-x

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