Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Mar 29;7(1):382.
doi: 10.1038/s42003-024-06080-1.

Insights on E1-like enzyme ATG7: functional regulation and relationships with aging-related diseases

Affiliations
Review

Insights on E1-like enzyme ATG7: functional regulation and relationships with aging-related diseases

Jingwei Liu et al. Commun Biol. .

Abstract

Autophagy is a dynamic self-renovation biological process that maintains cell homeostasis and is responsible for the quality control of proteins, organelles, and energy metabolism. The E1-like ubiquitin-activating enzyme autophagy-related gene 7 (ATG7) is a critical factor that initiates classic autophagy reactions by promoting the formation and extension of autophagosome membranes. Recent studies have identified the key functions of ATG7 in regulating the cell cycle, apoptosis, and metabolism associated with the occurrence and development of multiple diseases. This review summarizes how ATG7 is precisely programmed by genetic, transcriptional, and epigenetic modifications in cells and the relationship between ATG7 and aging-related diseases.

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Atg7 gene conservation among common species.
Atg7 is highly conserved among different species.
Fig. 2
Fig. 2. Classical autophagy process mediated by ATG7 as E1-like enzyme.
ATG7 protein is a homodimeric E1 enzyme that mediates covalent modifications of other autophagy-related proteins during autophagy, including the binding of ATG5 and ATG12, and the lipidation of LC3.
Fig. 3
Fig. 3. p53/Sirt1/ATG7 axis and ATG7 epigenetic modification.
It has been reported that ATG7 is regulated by epigenetic modifications of acetylation, deacetylation, and ubiquitination. p53/miR-155/Sirt1 axis forms a autophagy-regulating loop with ATG7.
Fig. 4
Fig. 4. An overview of ATG7 function and regulatory mechanism.
ATG7 is regulated at DNA, mRNA, and protein levels, and is closely associated with transcription regulation, cell fate, energy metabolism, developmental regulation and aging diseases.

Similar articles

Cited by

References

    1. Mizushima N, et al. A protein conjugation system essential for autophagy. Nature. 1998;395:395–398. doi: 10.1038/26506. - DOI - PubMed
    1. Levy JMM, Towers CG, and, Thorburn A. Targeting autophagy in cancer. Nat. Rev. Cancer. 2017;17:528–542. doi: 10.1038/nrc.2017.53. - DOI - PMC - PubMed
    1. Parzych KR, Klionsky DJ. An overview of autophagy: morphology, mechanism, and regulation. Antioxid. Redox Signal. 2014;20:460–473. doi: 10.1089/ars.2013.5371. - DOI - PMC - PubMed
    1. Levine B, Kroemer G. Biological functions of autophagy genes: a disease perspective. Cell. 2019;176:11–42. doi: 10.1016/j.cell.2018.09.048. - DOI - PMC - PubMed
    1. Kaiser SE, et al. Noncanonical E2 recruitment by the autophagy E1 revealed by Atg7-Atg3 and Atg7-Atg10 structures. Nat. Struct. Mol. Biol. 2012;19:1242–1249. doi: 10.1038/nsmb.2415. - DOI - PMC - PubMed

Publication types

MeSH terms

Substances