biostudies-literatureSahoo PKDr. Miriam and Sheldon G. Adelson Medical Research FoundationMerkin Peripheral Neuropathy and Nerve Regeneration CenterHHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)University of South Carolina Vice President for Research OfficeSouth Carolina Spinal Cord Injury Research FundSouth Carolina Spinal Cord Injury Research Fund (SCIRF)Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF)HHS | NIH | National Institute of Neurological Disorders and StrokeGeorge W. Neilson FoundationNINDS NIH HHSe2411811122https://www.ebi.ac.uk/biostudies/studies/S-EPMC11892601biostudies-literatureUnknown122(9)Depletion or inhibition of core stress granule proteins, G3BP1 in mammals and TIAR-2 in <i>Caenorhabditis elegans</i>, 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 (rodenProceedings of the National Academy of Sciences of the United States of AmericaDisruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.PMC11892601N/AR01-NS0117821733151R01 NS117821Hanovice NTwiss JLSahoo PKDesai MWard PJBenowitz LIDulin JNTuszynski MHSmith TPVaughn LSEnglish AWAgrawal MSiMa HHoule JDWelshhans KfalseDisruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.Depletion or inhibition of core stress granule proteins, G3BP1 in mammals and TIAR-2 in <i>Caenorhabditis elegans</i>, 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 (roden2025-01-01T00:00:00Z2025 Mar2026-06-01T18:01:28.876Z2025-04-04T02:54:28.158ZS-EPMC118926014001457310.1073/pnas.2411811122