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Last update 08 May 2025

ATG14

Last update 08 May 2025

Basic Info

Synonyms

ATG14, ATG14L, autophagy related 14

+ [4]

Introduction

Required for both basal and inducible autophagy. Determines the localization of the autophagy-specific PI3-kinase complex PI3KC3-C1 (PubMed:18843052, PubMed:19050071). Plays a role in autophagosome formation and MAP1LC3/LC3 conjugation to phosphatidylethanolamine (PubMed:19270696, PubMed:20713597). Promotes BECN1 translocation from the trans-Golgi network to autophagosomes (PubMed:20713597). Enhances PIK3C3 activity in a BECN1-dependent manner. Essential for the autophagy-dependent phosphorylation of BECN1 (PubMed:23878393). Stimulates the phosphorylation of BECN1, but suppresses the phosphorylation PIK3C3 by AMPK (PubMed:23878393). Binds to STX17-SNAP29 binary t-SNARE complex on autophagosomes and primes it for VAMP8 interaction to promote autophagosome-endolysosome fusion (PubMed:25686604, PubMed:37632749). Modulates the hepatic lipid metabolism (By similarity).

Drugs associated with ATG14

Autophagy inhibitors(University of Illinois)

Target

ATG14 x beclin-1

Mechanism

ATG14 modulators [+2]

Active Org.

Purdue University Center for Cancer Research [+1]

Originator Org.

University of Illinois [+1]

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ATG14

100 Translational Medicine associated with ATG14

0 Patents (Medical) associated with ATG14

423

Literatures (Medical) associated with ATG14

01 Aug 2025·Microbiological Research

A phloem-limited unculturable bacterium induces mild xenophagy in insect vectors for persistent infection

Article

Author: Yu, Zhongkai ; Guo, Yuxin ; Chen, Qian ; Wei, Taiyun ; Chen, Hongyan ; Wan, Wenqiang ; Hu, Mengting ; Li, You

Xenophagy is an important antibacterial defense mechanism that many organisms use to engulf intracellular pathogens. However, the mechanisms of xenophagy triggered by insect-borne plant bacteria are not well understood. Candidatus Liberibacter asiaticus (CLas) causes Huanglongbing, which poses a serious threat to citrus production. CLas is a phloem-limited unculturable bacterium that is transmitted by the Asian citrus psyllid in a persistent and propagative manner in nature. Here, we found that CLas infection in the gut of psyllids triggered a mild and anti-bacterial xenophagy. Xenophagy limited excessive propagation of CLas to maintain psyllid survival, because overload of CLas was detrimental to psyllid life. Furthermore, the outer membrane β-barrel protein (OMBB) of CLas is the key secreted protein that induces xenophagy in psyllids by interacting with ATG8 and ATG14. OMBB can independently induce autophagy in psyllid and non-host cells. Together, these results revealed that an insect-borne plant bacterium activates mild xenophagy to control its propagation, thereby achieving persistent infection in insect vectors.

01 Mar 2025·Journal of Biological Chemistry

USP1 promotes pancreatic cancer progression and autophagy by deubiquitinating ATG14

Article

Author: Zhang, Tao ; Dong, Hao ; Li, Jing ; Li, Leilei ; Fan, Zhili ; Liu, Ying ; Liu, Mengfei ; Gu, Xinyu ; Song, Zan ; Zhang, Zhicheng ; Li, Yu

Pancreatic ductal adenocarcinoma (PDAC) is characterized by extremely poor prognosis, high mortality, and limited therapeutic strategy. Autophagy is hyperactivated in PDAC, and targeting autophagy is emerging as a promising therapeutic strategy. The dysfunction of deubiquitinase ubiquitin-specific peptidase 1 (USP1) results in tumorigenesis and chemotherapy resistance. However, little is known about how USP1 regulates autophagy and its mechanism in tumor progression and drug sensitivity in PDAC. In this study, we found USP1 elevated in pancreatic cancer and USP1 expression inversely correlated with overall survival. USP1 depletion inhibited cell proliferation, epithelial-mesenchymal transition, and migration in PDAC cells. Interestingly, USP1 knockdown or inhibition reduced autophagy initiation and autophagy flux. By screening of interacting protein using coimmunoprecipitation, we identified that USP1 interacted with ATG14 (autophagy-related gene 14) protein, acting as a core component in autophagy initiation. Furthermore, USP1 overexpression deubiquitinated and enhanced ATG14 protein stability by reduced binding ubiquitin levels, whereas USP1 inhibition promoted its proteasome-dependent degradation. Notably, USP1 depletion or a novel USP1 inhibitor I-138 dramatically delayed tumor growth in xenograft model. USP1 inhibitor synergistically enhanced the anticancer efficiency of cisplatin in PDAC cells. Collectively, our study identifies USP1 as the first deubiquitinase in the modulation of ATG14 deubiquitination and unveils a regulatory role for USP1 in autophagy and PDAC progression. Targeting USP1 using a selective inhibitor I-138 may provide an effective strategy for chemotherapy treatment and combating drug resistance in autophagy-activated pancreatic cancer.

01 Feb 2025·Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

MEHP induced mitochondrial damage by promoting ROS production in CIK cells, leading to apoptosis, autophagy, cell cycle arrest

Article

Author: Han, Bing ; Lin, Hongjin ; Li, Wan ; Liu, Yufeng ; Li, Lu ; Yu, Yanbo

Although Mono (2-ethylhexyl) phthalate (MEHP) is a metabolite of Di (2-ethylhexyl) phthalate (DEHP), it has been confirmed to exhibit stronger biological toxicity than DEHP. Mitochondrial dynamic homeostasis and normal mitochondrial function regulate numerous physiological and pathological processes. However, it remains unclear whether MEHP triggers apoptosis, autophagy, and cell cycle arrest in grass carp kidney (CIK) cells by causing mitochondrial damage. Here, we established a MEHP dose-dependent exposure models in CIK cells and treated them with NAC. The results demonstrated that MEHP promoted ROS production and decreased antioxidant enzyme activities in CIK cells in a concentration-dependent manner. MEHP destroyed mitochondrial homeostasis and mitochondrial function in CIK cells, manifested by decreasing mitochondrial membrane potential (MMP), down-regulating gene expression of fusion division genes including MFN1, MFN2, CLPP, DRP1, OPA1, and MFF, and reducing OXPHOS complex enzyme protein level including COXI, COXII, COXIII, COXIV, and COXV. In addition, MEHP treatment not only can increase the level of Cyt-c, Atg12, Atg13, Atg14, Beclin1, ULK1, LC3-II, Caspase3, Caspase9, and Bax, but also can decrease the level of Bcl2, p62, CyclinB, CyclinD, and CyclinE in a concentration-dependent manner, which resulted in apoptosis, autophagy and cell cycle arrest. Furthermore, MEHP dose-dependently nduced downregulation gene expression of immunoglobulins and antimicrobial peptides (Hepcidin, β-defensin, LEAP2). However, NAC treatment could significantly reverse the above changes and alleviate CIK cells damage caused by exposure to MEHP. This study has expanded our understanding about molecular mechanisms of MEHP toxicity in aquatic animals and provided a reference for comparative medicine research.

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ATG14

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