Evidence map›Paper›PMID 27528605›Full record

ArticleThe Journal of biological chemistry2016

BNIP3 Protein Suppresses PINK1 Kinase Proteolytic Cleavage to Promote Mitophagy.

Tongmei Zhang, Liang Xue, Li Li, Chengyuan Tang, Zhengqing Wan, Ruoxi Wang, Jieqiong Tan, Ya Tan, Hailong Han, Runyi Tian and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
14.8field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 276 citations in OpenAlex.

  1. Pooled it
  2. Xenogeneic Mitochondrial Transplantation Improves Selected Age-Associated Phenotypes in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  8. Article
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  11. Article
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  16. Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Review

106 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 2 countries.

Tongmei ZhangFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Liang Xuethe Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907.
Li LiFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Chengyuan TangFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Zhengqing WanFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Ruoxi WangFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Jieqiong TanFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Ya TanFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Hailong HanFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Runyi TianFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
Timothy R BilliarFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
W Andy Taothe Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907.
Zhuohua ZhangFrom the Institute of Precision Medicine, the Xiangya Hospital and State Key Laboratory of Medical Genetics, the Xiangya Medical School, Central South University, Changsha, Hunan 410078, China zhangzhuohua@sklmg.edu.cn.
Central South University · CNPurdue University West Lafayette · USShanghai Center for Brain Science and Brain-Inspired Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in PINK1 (PTEN-induced putative kinase 1) cause early onset familial Parkinson's disease (PD). PINK1 accumulates on the outer membrane of damaged mitochondria followed by recruiting parkin to promote mitophagy. Here, we demonstrate that BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3), a mitochondrial BH3-only protein, interacts with PINK1 to promote the accumulation of full-length PINK1 on the outer membrane of mitochondria, which facilitates parkin recruitment and PINK1/parkin-mediated mitophagy. Inactivation of BNIP3 in mammalian cells promotes PINK1 proteolytic processing and suppresses PINK1/parkin-mediated mitophagy. Hypoxia-induced BNIP3 expression results in increased expression of full-length PINK1 and mitophagy. Consistently, expression of BNIP3 in Drosophila suppresses muscle degeneration and the mitochondrial abnormality caused by PINK1 inactivation. Together, the results suggest that BNIP3 plays a vital role in regulating PINK1 mitochondrial outer membrane localization, the proteolytic process of PINK1 and PINK1/parkin-mediated mitophagy under physiological conditions. Functional up-regulation of BNIP3 may represent a novel therapeutic strategy to suppress the progression of PD.

Indexed as

Gene Expression RegulationMitophagyAnimalsCell HypoxiaHEK293 CellsHeLa CellsHumansMembrane ProteinsMice, KnockoutMitochondrial MembranesMitochondrial ProteinsParkinson DiseaseProtein KinasesProto-Oncogene ProteinsPTEN-Induced Putative KinaseBNIP3 protein, humanBNip3 protein, mouseMembrane ProteinsMitochondrial ProteinsProtein KinasesProto-Oncogene ProteinsPTEN-Induced Putative KinasehypoxiamitochondriaparkinParkinson's diseaseubiquitin

Identifiers

PMID27528605
PMCPMC5076832
OpenAlexW2516249919

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.