STAT3 as a new autophagy regulator.
STAT3 as a new autophagy regulator.
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DOI：
10.4161/jkst.24353
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发表时间：
2013-07-01
期刊：
影响因子：
--
通讯作者：
Coqueret O
中科院分区：
文献类型：
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作者：
Jonchère B;Bélanger A;Guette C;Barré B;Coqueret O
信号转导和转录激活子3(STAT3)蛋白是一类细胞质转录因子，在生长因子或细胞因子刺激下转位到细胞核内诱导转录。除了正常功能外，这些蛋白还通过异常激活细胞周期进程和解除对生存和衰老途径的调控，在癌细胞中发挥重要作用。从Guido Kroemer的实验室获得的新数据表明，STAT3是一种新的自噬调节因子。在细胞质中，在没有酪氨酸705残基的常规磷酸化的情况下，STAT3与PKR激酶相互作用，抑制eIF2A的磷酸化，从而减少自噬途径。STAT3这种新的和非常规的功能在正常细胞中具有重要的作用，但我们认为它也可能影响癌细胞和对化疗的反应。
Signal transducers and activators of transcription 3 (STAT3) proteins are cytoplasmic transcription factors that translocate into the nucleus to induce transcription following growth factor or cytokine stimulation. Besides their normal functions, these proteins play an important role in cancer cells through the abnormal activation of cell cycle progression and the deregulation of survival and senescence pathways. New data obtained from the laboratory of Guido Kroemer identifies STAT3 as a new autophagy regulator. In the cytoplasm, in the absence of conventional phosphorylation on the tyrosine 705 residue, STAT3 interacts with the PKR kinase to inhibit eIF2A phosphorylation and so reduce autophagic pathways. This new and nonconventional function of STAT3 has an important role in normal cells but we suggest that it might also affect cancer cells and the response to chemotherapy treatment.