Mitochondrial STAT3: Powering up a potent factor

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• 作者：Daniel J. Garama ; Christine L. White ; Jesse J. Balic ; Daniel J. Gough ; ^{daniel.gough@hudson.org.au" class="auth_mail" title="E-mail the corresponding author}
• 关键词：EGF ; epidermal growth factor ; ETC ; Electron Transport Chain ; GAS ; γ-activated sequence ; IκB ; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor ; JAK ; Janus Kinase ; LIF ; leukemia inhibitory factor ; NF-κB ; nuclear factor kappa-light-chain-enhancer of activated B cells ; mPTP ; mitochondrial permeability transition pore ; PDGF ; platelet-derived growth factor ; SOCS ; Suppressors of Cytokine Signaling ; STAT ; Signal Transducer and Activator of Transcription ; TIM ; Transporter Inne
• 刊名：Cytokine
• 出版年：2016
• 出版时间：November 2016
• 年：2016
• 卷：87
• 期：Complete
• 页码：20-25
• 全文大小：1086 K

文摘

The JAK-STAT3 signaling pathway is engaged by many cytokines and growth factor stimuli to control diverse biological processes including proliferation, angiogenesis, survival, immune modulation, and metabolism. For over two decades it has been accepted that STAT3-dependent biology is due to its potency as a transcription factor capable of regulating the expression of many hundreds of genes. However, recent evidence of non-canonical and non-genomic activities of STAT3 has emerged. The most exciting of these activities is its capacity to translocate into the mitochondria where it regulates the activity of the electron transport chain and the opening of the mitochondrial permeability transition pore. These have broad consequences including cell survival and the production of reactive oxygen species and ATP in both normal tissue and under pathological conditions. Despite these fascinating observations there are many key unanswered questions about the mechanism of STAT mitochondrial activity.