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We further showed that CCP5 loss leads to an important hyperglutamylation that is paralleled with the loss of glycylation, highlighting the competition between these two PTMs, as previously described for mice lacking glycylation in the retina (Grau et al, 2017) (Fig

Damage-associated molecular patterns, such as high mobility group box 1 (HMGB1), initiate this phenotypic shift by engaging signaling pathways like toll-like receptor 4 (TLR4) and the receptor for advanced glycation end products (RAGE), which in turn activate downstream effectors, including nuclear factor kappa-B (NF-B) and the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome (Tastan and Heneka, 2024

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