Evidence map›Paper›PMID 27305174›Full record

ArticleAutophagy2016

PRKAA/AMPK restricts HBV replication through promotion of autophagic degradation.

Na Xie, Kefei Yuan, Li Zhou, Kui Wang, Hai-Ning Chen, Yunlong Lei, Jiang Lan, Qinqin Pu, Wei Gao, Lu Zhang and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. NIBV Induces Incomplete Autophagy via AMPK-TFEB, Causing Kidney Injury in Chicks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 9 institutions in 3 countries.

Na Xiea State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Kefei Yuana State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Li Zhoua State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Kui Wanga State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Hai-Ning Chenc Department of General Surgery , West China Hospital, Sichuan University , Chengdu , China.
Yunlong Leid Department of Biochemistry and Molecular Biology , and Molecular Medicine and Cancer Research Center, Chongqing Medical University , Chongqing , China.
Jiang Lana State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Qinqin Pua State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Wei Gaoa State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Lu Zhanga State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Guobo Shena State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Qifu Lib Department of Neurology , the Affiliated Hospital of Hainan Medical College , Haikou , China.
Hengyi Xiaoe Lab for Aging Research, Center for Medical Stem Cell Biology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University , Chengdu , China.
Hong Tangf Center of Infectious Diseases, West China Hospital, Sichuan University , Chengdu , Sichuan , China.
Rong Xiangg School of Medicine, Nankai University , Tianjin , China.
Mingliang Heh Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong , Hong Kong , China.
Pinghui Fengi Department of Molecular Microbiology and Immunology , Norris Comprehensive Cancer Center, University of Southern California , Los Angeles , CA , USA.
Edouard C Nicej Department of Biochemistry and Molecular Biology , Monash University , Clayton , Victoria , Australia.
Yuquan Weia State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Haiyuan Zhangb Department of Neurology , the Affiliated Hospital of Hainan Medical College , Haikou , China.
Jiayin Yangk Department of Liver Surgery , West China Hospital, Sichuan University , Chengdu , China.
Canhua Huanga State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy , Chengdu , China.
Sichuan University · CNState Key Laboratory of BiotherapyHainan Medical College Hospital · CNChinese University of Hong Kong · CNChongqing Medical University · CNMonash University · AUNankai University · CNUniversity of Southern California · USWest China Hospital of Sichuan University · CN

Funding

Targeting an immune kinase to purge KSHV latent infectionR01DE026003 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, CASEY, ZHANG, CHAO · 2016 to 2020
$3.4M
NIDCR NIH HHS R01 DE026003
6 · The paper itself

Abstract

Adenosine monophosphate-activated protein kinase (AMPK) is a crucial energy sensor that maintains cellular energy homeostasis. AMPK plays a critical role in macroautophagy/autophagy, and autophagy facilitates hepatitis B virus (HBV) replication. To date, the intrinsic link among AMPK, autophagy and HBV production remains to be elucidated. Here, we demonstrate that PRKAA (a catalytic subunit of AMPK) is activated in response to HBV-induced oxidative stress, which in turn decreases the production of HBV. Mechanistic studies reveal that the autophagy machinery is associated with the inhibitory effect of PRKAA/AMPK on HBV production. Activation of PRKAA/AMPK promotes autolysosome-dependent degradation through stimulation of cellular ATP levels, which then leads to the depletion of autophagic vacuoles. Taken together, our data suggest that the activation of AMPK might be a stress response of host cells to restrict virus production through promotion of autophagic degradation. These findings therefore indicate that AMPK could provide a potential therapeutic target for HBV infection.

Indexed as

Virus ReplicationAdenosine TriphosphateAMP-Activated Protein KinasesAnimalsAutophagyDNA ReplicationEnzyme ActivationGreen Fluorescent ProteinsHepatitis B virusHep G2 CellsHumansHydrogen-Ion ConcentrationLysosomesMaleMiceMice, Inbred BALB CAdenosine TriphosphateAMP-Activated Protein KinasesGreen Fluorescent ProteinsMicrotubule-Associated ProteinsOligonucleotidesPRKAA1 protein, humanReactive Oxygen SpeciesRNA, Small InterferingTOR Serine-Threonine Kinasesadenosine monophosphate-activated protein kinaseadenosine triphosphateautophagyhepatitis B virusoxidative stress

Identifiers

PMID27305174
PMCPMC5082782
OpenAlexW2422314397

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.