| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6022394 | Neurobiology of Disease | 2013 | 11 Pages |
Abstract
⺠Increased CNTF in the SVZ mediates stroke-induced SVZ neurogenesis. ⺠CNTF may act indirectly through FGF2 to increase progenitor (C cell) proliferation. ⺠Inflammatory cytokines, like TNFα, seem to counteract pro-neurogenic CNTF effects. ⺠In mice, stroke-induced proliferation develops slowly under very specific conditions. ⺠Nervous system-selective expression of CNTF might make it a good indirect drug target.
Keywords
EGFRLIFDelta-like 3Dll3MASH1gp130IFNγCD45Hes5FGF2Msi1MCAOIGF-1CNTFEPOCorpus callosumKi67EGFPBSECAMCAIgGIL-65-bromo-2′-deoxyuridineBDNFerythropoietinmiddle cerebral artery occlusionimmunoglobulin Ginterferon-gammainterleukin-6phosphate bufferBrdUlateral ventriclemiddle cerebral arteryexternal carotid arteryepidermal growth factorfibroblast growth factor 2leukemia inhibitory factorinsulin-like growth factor 1Brain-derived neurotrophic factorciliary neurotrophic factorMusashi-1hairy and enhancer of split 1Hes1glycoprotein 130Epidermal growth factor receptor
Related Topics
Life Sciences
Neuroscience
Neurology
Authors
Seong Su Kang, Matthew P. Keasey, Sheila A. Arnold, Rollie Reid, Justin Geralds, Theo Hagg,