Cross-talk between KLF4 and STAT3 regulates axon regeneration.

Cytokine-induced activation of signal transducer and activator of transcription 3 promotes the regrowth of damaged axons in the adult central nervous system (CNS). Here we show that KLF4 physically interacts with upon cytokine-induced phosphorylation of tyrosine 705 (Y705) on This interaction suppresses 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 signalling. This regeneration can be greatly enhanced by exogenous cytokine treatment, or removal of an endogenous pathway inhibitor called suppressor of cytokine signalling 3 (SOCS3). These findings reveal an unexpected cross-talk between KLF4 and activated duanyu18133 in the regulation of axon regeneration that might have therapeutic implications in promoting repair of injured adult CNS.

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