4.8 Editorial Material

Release the autophage brake on inflammation: The MAPK14/p38 alpha-ULK1 pedal

Journal

AUTOPHAGY
Volume 14, Issue 6, Pages 1097-1098

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2018.1446626

Keywords

autophagy; inflammation; MAPK14/p38 alpha; microglia; ULK1

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Funding

  1. BrightFocus Foundation [A2016501S]
  2. National Institutes of Health [NS079858, NS095269, AG023695, P50 AG025688]
  3. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS095269] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE ON AGING [P50AG025688] Funding Source: NIH RePORTER

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Macroautophagy/autophagy and inflammation are 2 intertwined processes vital for immune cells to perform their functions. Under resting conditions, autophagy acts as a brake to suppress inflammation in microglia. Upon signal stimulation, their fine-tuned interplay is pivotal for proper response to stress. How inflammatory signals remove this autophagy brake on inflammation remains unclear. In a recent study, we showed that the stress kinase MAPK14/p38 alpha in microglia senses the inflammatory cue lipopolysaccharide (LPS), directly phosphorylates and inhibits ULK1, relieves the autophagic inhibition on the inflammatory machinery, and thus allows for a full immune response.

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