Publication | Open Access
STAT3 as a new autophagy regulator
47
Citations
32
References
2013
Year
MitophagySignal TransducersImmunologyCell DeathCell AutophagySignaling PathwayCell RegulationReceptor Tyrosine KinaseAutophagyPkr KinaseLipophagyCell SignalingNew Autophagy RegulatorJak-stat Signaling PathwayAutoimmune DiseaseMolecular PathwayAutoimmunityTranscription 3Cell BiologyTumor MicroenvironmentSignal TransductionAutoantibody ProductionSystems BiologyMedicine
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.
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