The mammalian ULK1 complex and autophagy initiation

Maria Zachari, Ian G. Ganley (Lead / Corresponding author)

Research output: Contribution to journalReview articlepeer-review

155 Citations (Scopus)
203 Downloads (Pure)

Abstract

Autophagy is a vital lysosomal degradation pathway that serves as a quality control mechanism. It rids the cell of damaged, toxic or excess cellular components, which if left to persist could be detrimental to the cell. It also serves as a recycling pathway to maintain protein synthesis under starvation conditions. A key initial event in autophagy is formation of the autophagosome, the unique double-membrane organelle that engulfs the cytosolic cargo destined for degradation. This step is mediated by the serine/threonine protein kinase ULK1, which functions in a complex with at least three protein partners: FIP200, ATG13, and ATG101. In this chapter, we will focus on the regulation of the ULK1 complex during autophagy initiation. The complex pattern of upstream pathways that converge on ULK1 suggests that this complex acts as a node, converting multiple signals into autophagosome formation. Here we will review our current understanding of this regulation and in turn discuss what happens downstream, once the ULK1 complex becomes activated.
Original languageEnglish
Pages (from-to)585-596
Number of pages12
JournalEssays in Biochemistry
Volume61
Issue number6
DOIs
Publication statusPublished - 12 Dec 2017

Keywords

  • Autophagy
  • ULK1
  • ATG13
  • FIP200
  • ATG101
  • mTOR
  • Kinase
  • Autophagosome
  • Phagophore

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