{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sahoo PK"],"funding":["Dr. Miriam and Sheldon G. Adelson Medical Research Foundation","Merkin Peripheral Neuropathy and Nerve Regeneration Center","HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)","University of South Carolina Vice President for Research Office","South Carolina Spinal Cord Injury Research Fund","South 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 Stroke","George W. Neilson Foundation","NINDS NIH HHS"],"pagination":["e2411811122"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11892601"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122(9)"],"pubmed_abstract":["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 (roden"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration."],"pmcid":["PMC11892601"],"funding_grant_id":["N/A","R01-NS0117821","733151","R01 NS117821"],"pubmed_authors":["Hanovice N","Twiss JL","Sahoo PK","Desai M","Ward PJ","Benowitz LI","Dulin JN","Tuszynski MH","Smith TP","Vaughn LS","English AW","Agrawal M","SiMa H","Houle JD","Welshhans K"],"additional_accession":[]},"is_claimable":false,"name":"Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.","description":"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 (roden","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-01T18:01:28.876Z","creation":"2025-04-04T02:54:28.158Z"},"accession":"S-EPMC11892601","cross_references":{"pubmed":["40014573"],"doi":["10.1073/pnas.2411811122"]}}