Bio News
A study found that K11 lactylation and S199 phosphorylation of B-type creatine kinase (CKB) showed neuroprotective effects in ischemia-reperfusion injury after stroke. S199 phosphorylation recruited the acetyltransferase GCN5 to promote K11 lactylation, which increased CKB enzyme activity and suppressed reactive oxygen species. In a mouse model, disrupting K11 lactylation or S199 phosphorylation reduced CKB function, worsened neuronal damage and delayed recovery after stroke.
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biobookmedia@biobook.co.krRoche’s New Drug for Uveitic Macular Edema Faces FDA Decision in July 2027
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