Vol.44, No.4, 2020, pp.535-543, doi:10.32604/biocell.2020.09171
OPEN ACCESS
REVIEW
Functions of ULK1 in autophagy and non-autophagy pathways and its implications in human physiology and disease
  • LINNA TAN1,2, YUYONG TAN1,2, DELIANG LIU1,2,*
1 Department of Gastroenterology, the Second Xiangya Hospital, Changsha, 410011, China
2 Research Center of Digestive Disease, Central South University, Changsha, 410011, China
* Address correspondence to: Deliang Liu,
Received 18 November 2019; Accepted 28 April 2020; Issue published 24 December 2020
Abstract
ULK1 (unc-51 like autophagy activating kinase 1), a mammalian serine/threonine kinase, is a key component of autophagy initiation complex and helps to induce all types of autophagy. Canonical autophagy is a process in which, through the interactions of a series of autophagy-related proteins, damaged organelles or misfolded proteins are engulfed by autophagosomes and then merged with lysosomes to be degraded. Thus, canonical autophagy is an important constituent part of the cellular “quality control.” Besides, accumulating evidence indicates that ULK1 exerts autophagy-independent effects in a cell-specific manner. For example, ULK1 facilitates neurite elongation through the regulation of endoplasmic reticulum (ER)–Golgi trafficking in neurons, stimulates phosphopentose pathway to help NADPH (nicotinamide adenine dinucleotide phosphate hydrogen) production, and acts as a duplex regulator in type I IFN (type I interferon) induced innate immune response. Considering the importance and diversity of ULK1 in various biological processes, this review aims to present a comprehensive overview of autophagy and non-autophagy related functions of ULK1 in a variety of human physiological, pathological, and disease processes.
Keywords
Ubiquitination, Axonal extension, Cancer, Metabolism, Immune response, Stress
Cite This Article
TAN, L., TAN, Y., LIU, D. (2020). Functions of ULK1 in autophagy and non-autophagy pathways and its implications in human physiology and disease. BIOCELL, 44(4), 535–543.
Citations
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