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BRENDA support

Literature summary for 2.3.1.108 extracted from

  • Wang, B.; Rao, Y.H.; Inoue, M.; Hao, R.; Lai, C.H.; Chen, D.; McDonald, S.L.; Choi, M.C.; Wang, Q.; Shinohara, M.L.; Yao, T.P.
    Microtubule acetylation amplifies p38 kinase signalling and anti-inflammatory IL-10 production (2014), Nat. Commun., 5, 3479.
    View publication on PubMedView publication on EuropePMC

Activating Compound

Activating Compound Comment Organism Structure
lipopolysaccharide macrophages challenged by bacterial lipopolysaccharides undergo extensive microtubule acetylation Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
RAW-264.7 cell
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Mus musculus
-

General Information

General Information Comment Organism
physiological function macrophages challenged by bacterial lipopolysaccharides undergo extensive microtubule acetylation. Suppression of lipopolysaccharide-induced microtubule acetylation by inactivating the tubulin acetyltransferase, MEC17, profoundly inhibits the induction of anti-inflammatory interlukin-10, a phenotype effectively reversed by an acetylation-mimicking alpha-tubulin mutant. Reversible microtubule acetylation is a kinase signaling modulator and a key component in the inflammatory response Mus musculus