| First Author | Qin S | Year | 2013 |
| Journal | Nat Commun | Volume | 4 |
| Pages | 2633 | PubMed ID | 24129709 |
| Mgi Jnum | J:206059 | Mgi Id | MGI:5547847 |
| Doi | 10.1038/ncomms3633 | Citation | Qin S, et al. (2013) Cross-talk between KLF4 and STAT3 regulates axon regeneration. Nat Commun 4:2633 |
| abstractText | Cytokine-induced activation of signal transducer and activator of transcription 3 (STAT3) promotes the regrowth of damaged axons in the adult central nervous system (CNS). Here we show that KLF4 physically interacts with STAT3 upon cytokine-induced phosphorylation of tyrosine 705 (Y705) on STAT3. This interaction suppresses STAT3-dependent gene expression by blocking its DNA-binding activity. The deletion of KLF4 in vivo induces axon regeneration of adult retinal ganglion cells (RGCs) via Janus kinase (JAK)-STAT3 signalling. This regeneration can be greatly enhanced by exogenous cytokine treatment, or removal of an endogenous JAK-STAT3 pathway inhibitor called suppressor of cytokine signalling 3 (SOCS3). These findings reveal an unexpected cross-talk between KLF4 and activated STAT3 in the regulation of axon regeneration that might have therapeutic implications in promoting repair of injured adult CNS. |
