{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ozkan A"],"funding":["McKnight Brain Research Institute","NINDS NIH HHS"],"pagination":["RP100340"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12844902"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Corticospinal neurons (CSN) centrally degenerate in amyotrophic lateral sclerosis (ALS), along with spinal motor neurons, and loss of voluntary motor function in spinal cord injury (SCI) results from damage to CSN axons. For functional regeneration of specifically affected neuronal circuitry <i>in vivo</i>, or for optimally informative disease modeling and/or therapeutic screening <i>in vitro</i>, it is important to reproduce the type or subtype of neurons involved. No such appropriate <i>in vitro</i> models exist with which to investigate CSN selective vulnerability and degeneration in ALS, or to investigate routes to regeneration of CSN circuitry for ALS or SCI, critically limiting the relevance of much research. Here, we identify that the HMG-domain transcription factor <i>Sox6</i> is e"],"journal":["eLife"],"pubmed_title":["Directed differentiation of functional corticospinal-like neurons from endogenous SOX6+/NG2+ cortical progenitors."],"pmcid":["PMC12844902"],"funding_grant_id":["Regeneration Project Fellowship","NS049553","NS045523","DP1 NS106665"],"pubmed_authors":["Shipman SL","Basak AN","Azim E","Sadegh C","Ozkan A","Padmanabhan HK","Kumar P","Macklis JD"],"additional_accession":[]},"is_claimable":false,"name":"Directed differentiation of functional corticospinal-like neurons from endogenous SOX6+/NG2+ cortical progenitors.","description":"Corticospinal neurons (CSN) centrally degenerate in amyotrophic lateral sclerosis (ALS), along with spinal motor neurons, and loss of voluntary motor function in spinal cord injury (SCI) results from damage to CSN axons. For functional regeneration of specifically affected neuronal circuitry <i>in vivo</i>, or for optimally informative disease modeling and/or therapeutic screening <i>in vitro</i>, it is important to reproduce the type or subtype of neurons involved. No such appropriate <i>in vitro</i> models exist with which to investigate CSN selective vulnerability and degeneration in ALS, or to investigate routes to regeneration of CSN circuitry for ALS or SCI, critically limiting the relevance of much research. Here, we identify that the HMG-domain transcription factor <i>Sox6</i> is e","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-15T08:51:16.25Z","creation":"2026-06-15T03:11:15.963Z"},"accession":"S-EPMC12844902","cross_references":{"pubmed":["41589677"],"doi":["10.7554/eLife.100340"]}}