{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schachtrup C"],"funding":["NINDS NIH HHS","NIGMS NIH HHS"],"pagination":["11814-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1913857"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["104(28)"],"pubmed_abstract":["Changes in the molecular and cellular composition of the CNS after injury or disease result in the formation of an inhibitory environment that inhibits the regeneration of adult mammalian CNS neurons. Although a dramatic change in the CNS environment after traumatic injury or disease is hemorrhage because of vascular rupture or leakage of the blood-brain barrier, the potential role for blood proteins in repair processes remains unknown. Here we show that the blood protein fibrinogen is an inhibitor of neurite outgrowth that is massively deposited in the spinal cord after injury. We show that fibrinogen acts as a ligand for beta3 integrin and induces the transactivation of EGF receptor (EGFR) in neurons. Fibrinogen-mediated inhibition of neurite outgrowth is reversed by blocking either beta"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Fibrinogen inhibits neurite outgrowth via beta 3 integrin-mediated phosphorylation of the EGF receptor."],"pmcid":["PMC1913857"],"funding_grant_id":["P30 NS047101","R01NS051470","R01 NS051470","R01NS052189","R01 NS052189","T32 GM007752","R01 NS054734"],"pubmed_authors":["Schachtrup C","Lu J","Lee JK","Zheng B","Akassoglou K","Jones LL","Lu P","Sachs BD"],"additional_accession":[]},"is_claimable":false,"name":"Fibrinogen inhibits neurite outgrowth via beta 3 integrin-mediated phosphorylation of the EGF receptor.","description":"Changes in the molecular and cellular composition of the CNS after injury or disease result in the formation of an inhibitory environment that inhibits the regeneration of adult mammalian CNS neurons. Although a dramatic change in the CNS environment after traumatic injury or disease is hemorrhage because of vascular rupture or leakage of the blood-brain barrier, the potential role for blood proteins in repair processes remains unknown. Here we show that the blood protein fibrinogen is an inhibitor of neurite outgrowth that is massively deposited in the spinal cord after injury. We show that fibrinogen acts as a ligand for beta3 integrin and induces the transactivation of EGF receptor (EGFR) in neurons. Fibrinogen-mediated inhibition of neurite outgrowth is reversed by blocking either beta","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Jul","modification":"2026-03-16T16:09:03.918Z","creation":"2019-03-27T02:04:20Z"},"accession":"S-EPMC1913857","cross_references":{"pubmed":["17606926"],"doi":["10.1073/pnas.0704045104"]}}