Evidence map›Paper›PMID 27050458›Full record

ArticleAutophagy2016

Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy.

Ming Chen, Ziheng Chen, Yueying Wang, Zheng Tan, Chongzhuo Zhu, Yanjun Li, Zhe Han, Linbo Chen, Ruize Gao, Lei Liu and 1 more

Abstract 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 349 papers.

0numbers the graph read from it
0cells of the map it votes in
349citing papers in PubMed
–field-weighted citation impact
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

349 citing papers in PubMed.

  1. Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026
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289 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

11 authors.

Ming Chena State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Ziheng Chena State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Yueying Wanga State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Zheng Tana State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Chongzhuo Zhua State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Yanjun Lia State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Zhe Hanc State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Science, College of Life Sciences, Nankai University , Tianjin , China.
Linbo Chenc State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Science, College of Life Sciences, Nankai University , Tianjin , China.
Ruize Gaoc State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Science, College of Life Sciences, Nankai University , Tianjin , China.
Lei Liua State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.
Quan Chena State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing , China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial fragmentation due to imbalanced fission and fusion of mitochondria is a prerequisite for mitophagy, however, the exact "coupling" of mitochondrial dynamics and mitophagy remains unclear. We have previously identified that FUNDC1 recruits MAP1LC3B/LC3B (LC3) through its LC3-interacting region (LIR) motif to initiate mitophagy in mammalian cells. Here, we show that FUNDC1 interacts with both DNM1L/DRP1 and OPA1 to coordinate mitochondrial fission or fusion and mitophagy. OPA1 interacted with FUNDC1 via its Lys70 (K70) residue, and mutation of K70 to Ala (A), but not to Arg (R), abolished the interaction and promoted mitochondrial fission and mitophagy. Mitochondrial stress such as selenite or FCCP treatment caused the disassembly of the FUNDC1-OPA1 complex while enhancing DNM1L recruitment to the mitochondria. Furthermore, we observed that dephosphorylation of FUNDC1 under stress conditions promotes the dissociation of FUNDC1 from OPA1 and association with DNM1L. Our data suggest that FUNDC1 regulates both mitochondrial fission or fusion and mitophagy and mediates the "coupling" across the double membrane for mitochondrial dynamics and quality control.

Indexed as

Mitochondrial DynamicsMitophagyAmino Acid SequenceCasein Kinase IIDynaminsGene Knockdown TechniquesGTP PhosphohydrolasesHeLa CellsHumansMembrane ProteinsMicrotubule-Associated ProteinsMitochondriaMitochondrial ProteinsPhosphorylationProtein BindingCasein Kinase IIDNM1L protein, humanDynaminsFUNDC1 protein, humanGTP PhosphohydrolasesMembrane ProteinsMicrotubule-Associated ProteinsMitochondrial ProteinsOPA1 protein, humanDNM1L/DRP1mitochondrial dynamicsmitophagymitophagy receptorOPA1

Identifiers

PMID27050458
PMCPMC4836026

What OpenQuestion holds

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Registered trials

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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.