Fig. 2: The Kla modifications of functional proteins in infectious diseases.
From: Lysine lactylation in diseases: beyond histone lactylation
Elevated lactate levels are observed in the microenvironment of some infectious diseases. In tissues with high lactate content, cGAS can be Kla-modified, leading its dysfunction to recognize dsDNA and the production of anti-infective cytokines. Besides, the Kla modification of RUBCN can promote the formation of LAPosome, thereby upregulating MHC Ⅱ to enhance immunological recognition. The Kla modification of IFI16 inhibits its interaction with DNA-PK and prevents the biogenesis of anti-infective cytokines to promote viral replication. KSHV can also induces the Kla modification of NAT10 to enhance stability of the RNA of KSHV, thereby facilitating viral replication. Furthermore, YTHDF1 and ALKBH5, the m6A writer and eraser, can also undergo Kla modifications, resulting in the mRNAs of IFNB1 and SFTSV NP stabilized to induce distinct effects.
