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Cross-talk between KLF4 and STAT3 regulates axon regeneration

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  • Song Qin

    (University of Texas Southwestern Medical Center)

  • Yuhua Zou

    (University of Texas Southwestern Medical Center)

  • Chun-Li Zhang

    (University of Texas Southwestern Medical Center)

Abstract

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.

Suggested Citation

  • Song Qin & Yuhua Zou & Chun-Li Zhang, 2013. "Cross-talk between KLF4 and STAT3 regulates axon regeneration," Nature Communications, Nature, vol. 4(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3633
    DOI: 10.1038/ncomms3633
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