Evidence map›Paper›PMID 30103670›Full record

ArticleAutophagy2018

Autosomal dominant retinitis pigmentosa-associated gene PRPF8 is essential for hypoxia-induced mitophagy through regulating ULK1 mRNA splicing.

Guang Xu, Ting Li, Jiayi Chen, Changyan Li, Haixin Zhao, Chengcheng Yao, Hua Dong, Kaiqing Wen, Kai Wang, Jie Zhao and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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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

16 authors at 3 institutions in 1 country.

Guang Xua State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Ting Lia State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Jiayi Chena State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Changyan Lib State Key Laboratory of Proteomics, Beijing Proteome Research Center , Beijing Institute of Lifeomics , Beijing , China.
Haixin Zhaoa State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Chengcheng Yaoa State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Hua Donga State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Kaiqing Wena State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Kai Wanga State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Jie Zhaoa State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Qing Xiaa State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Tao Zhoua State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Huafeng Zhangc Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences , University of Science and Technology of China , Hefei , China.
Ping Gaoc Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences , University of Science and Technology of China , Hefei , China.
Ailing Lia State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
Xin Pana State Key Laboratory of Proteomics, Institute of Basic Medical Sciences , National Center of Biomedical Analysis , Beijing , China.
National Center of Biomedical Analysis · CNUniversity of Science and Technology of China · CNBeijing Proteome Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aged and damaged mitochondria can be selectively degraded by specific autophagic elimination, termed mitophagy. Defects in mitophagy have been increasingly linked to several diseases including neurodegenerative diseases, metabolic diseases and other aging-related diseases. However, the molecular mechanisms of mitophagy are not fully understood. Here, we identify PRPF8 (pre-mRNA processing factor 8), a core component of the spliceosome, as an essential mediator in hypoxia-induced mitophagy from an RNAi screen based on a fluorescent mitophagy reporter, mt-Keima. Knockdown of PRPF8 significantly impairs mitophagosome formation and subsequent mitochondrial clearance through the aberrant mRNA splicing of ULK1, which mediates macroautophagy/autophagy initiation. Importantly, autosomal dominant retinitis pigmentosa (adRP)-associated PRPF8 mutant R2310K is defective in regulating mitophagy. Moreover, knockdown of other adRP-associated splicing factors, including PRPF6, PRPF31 and SNRNP200, also lead to ULK1 mRNA mis-splicing and mitophagy defects. Thus, these findings demonstrate that PRPF8 is essential for mitophagy and suggest that dysregulation of spliceosome-mediated mitophagy may contribute to pathogenesis of retinitis pigmentosa.

Indexed as

Genes, DominantAnimalsAutophagy-Related Protein-1 HomologGene Expression RegulationHeLa CellsHumansHypoxiaMiceMitophagyMutationPhagosomesRetinitis PigmentosaRNA-Binding ProteinsRNA InterferenceRNA, MessengerRNA SplicingAutophagy-Related Protein-1 HomologPrp8 protein, mousePRPF8 protein, humanRNA-Binding ProteinsRNA, MessengerRNA Splicing FactorsAutosomal dominant retinitis pigmentosahypoxiamitophagymRNA splicingPRPF8ULK1

Identifiers

PMID30103670
PMCPMC6135625
OpenAlexW2887341546

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.