Evidence map›Paper›PMID 29962275›Full record

ArticleCell cycle (Georgetown, Tex.)2018

HIV-1 Tat increases BAG3 via NF-κB signaling to induce autophagy during HIV-associated neurocognitive disorder.

Xiaoyan Wu, Huaqian Dong, Xiang Ye, Li Zhong, Tiantian Cao, Qiping Xu, Jun Wang, Yu Zhang, Jinhong Xu, Wei Wang and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Xiaoyan Wua Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Huaqian Donga Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Xiang Yea Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Li Zhonga Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Tiantian Caoa Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Qiping Xua Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Jun Wanga Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Yu Zhanga Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Jinhong Xua Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Wei Wangb Institute of Laboratory Animal Sciences of Chinese Academy of Medical Science , Beijing , China.
Qiang Weib Institute of Laboratory Animal Sciences of Chinese Academy of Medical Science , Beijing , China.
Ying Liuc State Key Laboratory for Infectious Disease Prevention and Control, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases , National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention , Beijing , China.
Shuhui Wangc State Key Laboratory for Infectious Disease Prevention and Control, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases , National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention , Beijing , China.
Yiming Shaoc State Key Laboratory for Infectious Disease Prevention and Control, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases , National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention , Beijing , China.
Huiqin Xinga Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pathology , Basic Medicine, Medical College, Xiamen University , Xiamen , China.
Xiamen University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human immunodeficiency virus-1 (HIV-1) regulatory protein Tat plays an important role during HIV-1-associated neurocognitive disorders (HAND) by inducing neuronal autophagy. In this study, we used immunohistochemistry, immunofluorescence, western blot, qRT-PCR, and RNA interference to elucidate the involvement of Bcl-2-associated athanogene 3 (BAG3) in the pathogenesis of HIV-1 Tat-induced autophagy during HAND. We found that BAG3 expression is elevated in astrocytes in frontal cortex of macaques infected with simian immunodeficiency virus-human immunodeficiency chimeric virus (SHIV). In addition, in human primary glioblastoma cells (U87), HIV-1 Tat upregulated BAG3 in an NF-κB-dependent manner to induce autophagy. Importantly, suppression of BAG3 or inhibition of NF-κB activity reversed the HIV-1 Tat-induced autophagy. These results indicate that HIV-1 Tat induces autophagy by upregulating BAG3 via NF-κB signaling, which suggests BAG3 and NF-κB could potentially serve as novel targets for HAND therapies.

Indexed as

AutophagySignal TransductionAdaptor Proteins, Signal TransducingAIDS Dementia ComplexAnimalsApoptosis Regulatory ProteinsAstrocytesCell Line, TumorFemaleHIV-1MacacaMaleNF-kappa BRNA, Viraltat Gene Products, Human Immunodeficiency VirusUp-RegulationAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanNF-kappa BRNA, Viraltat Gene Products, Human Immunodeficiency VirusautophagyBAG3HANDHIV-1 TatNF-κB

Identifiers

PMID29962275
PMCPMC6133340
OpenAlexW2810806536

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.