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. 2022 Feb 25;29(9):1744–1756. doi: 10.1038/s41418-022-00959-4

Fig. 8. A potential role of Crabp1 in protecting MN degeneration and maintaining healthy NMJ.

Fig. 8

A The scheme illustrates that deleting Crabp1 in mice results in an adult-onset, progressive MN degenerative phenotype with specific defects in the NMJ. B The scheme illustrates the mechanism of CRABP1-CaMKII-AGRIN signal in spinal MNs, which modulates downstream events in NMJ. Dysregulated CRABP1-CaMKII-Agrn signaling in spinal MNs leads to a disrupted nerve-muscle communication (disrupted AGRIN-LRP4-MuSK signaling and t-SNARE expression) in adult NMJ, and, subsequently, progressive NMJ deficits and a MN degenerative phenotype.