Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.

ABSTRACT: Depletion or inhibition of core stress granule proteins, G3BP1 in mammals and TIAR-2 in Caenorhabditis elegans, increases the growth of spontaneously regenerating axons. Inhibition of G3BP1 by expression of its acidic or "B-domain" accelerates axon regeneration after nerve injury, bringing a potential therapeutic strategy for peripheral nerve repair. Here, we asked whether G3BP1 inhibition is a viable strategy to promote regeneration in injured mammalian central nervous system (CNS) where axons do not regenerate spontaneously. G3BP1 B-domain expression was found to promote axon regeneration in the transected spinal cord provided with a permissive peripheral nerve graft (PNG) as well as in crushed optic nerve. Moreover, a cell-permeable peptide (CPP) to a subregion of B-domain (roden

SUBMITTER: Sahoo PK 

PROVIDER: S-EPMC11892601 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature