Noncatalytic functions of IPMK are essential for activation of autophagy and liver regeneration

Prasun Guha, Solomon H. Snyder

Research output: Contribution to journalComment/debatepeer-review

4 Scopus citations


Macroautophagy/autophagy plays important roles in health and disease, but mechanisms of its activation are unclear. Recently we established IPMK (inositol polyphosphate multikinase) as a physiological determinant of autophagy independent of its catalytic activity. Two signaling axes, IPMK-AMPK-SIRT1 and IPMK-AMPK-ULK1, appear to mediate the influence of IPMK on autophagy. IPMK enhances autophagy-related transcription by stimulating AMPK-dependent SIRT1 activation, which mediates the deacetylation of histone 4 lysine 16. Furthermore, direct binding of IPMK to ULK and AMPK forms a ternary complex that facilitates AMPK-dependent ULK phosphorylation. Deletion of Ipmk virtually abolishes lipophagy, promotes liver damage and impairs hepatocyte regeneration. Our study establishes the importance of IPMK in regulation of autophagy and as a drug target for autophagy-related diseases.

Original languageEnglish (US)
Pages (from-to)1473-1474
Number of pages2
Issue number8
StatePublished - Aug 3 2019


  • AMPK
  • IPMK (Inositol polyphosphate multikinase)
  • ULK
  • autophagy
  • liver

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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