Fig. 3: The Kla modifications of functional proteins in neurological diseases.
From: Lysine lactylation in diseases: beyond histone lactylation
The Kla modifications of functional proteins play both accelerative and suppressive roles in neurological diseases. The Kla-modified Tau can induce apoptosis and ferroptosis of neuron, thereby promoting the progression of AD. The Kla modification of Tufm can attenuate its interaction with Tomm40, inhibiting mitophagy to induce neuronal apoptosis. The vesicle-resident protein ARF can also be Kla-modified to inhibit the transmitting of healthy mitochondria from astrocytes to neurons, resulting in neuronal damage. On the contrary, the Kla modification of APP can inhibit the accumulation of Aβ, relieving the progression of AD. The Kla-modified SNAP91 can also promote vesicle formation and remodeling the shape of synapse to relieve anxiety disorder.
