Evidence map›Paper›PMID 26134044›Full record

ArticleMolecular and cellular biochemistry2015

The tRNA(Gly) T10003C mutation in mitochondrial haplogroup M11b in a Chinese family with diabetes decreases the steady-state level of tRNA(Gly), increases aberrant reactive oxygen species production, and reduces mitochondrial membrane potential.

Wei Li, Chaowei Wen, Weixing Li, Hailing Wang, Xiaomin Guan, Wanlin Zhang, Wei Ye, Jianxin Lu

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Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

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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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Novel mitochondrial tRNAWorld journal of pediatrics : WJP · 2020
    Article
  5. Review
  6. Review
  7. The Mitochondrial tRNABalkan journal of medical genetics : BJMG · 2018
    Article
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

8 authors at 2 institutions in 1 country.

Wei LiKey Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou, 325035, Zhejiang, People's Republic of China.
Chaowei WenKey Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou, 325035, Zhejiang, People's Republic of China.
Weixing LiDepartment of Laboratory Medicine, Zhejiang Provincial People's Hospital, Hangzhou, 310014, Zhejiang, People's Republic of China.
Hailing WangZhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou, 325035, Zhejiang, People's Republic of China.
Xiaomin GuanZhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou, 325035, Zhejiang, People's Republic of China.
Wanlin ZhangZhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou, 325035, Zhejiang, People's Republic of China.
Wei YeKey Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou, 325035, Zhejiang, People's Republic of China.
Jianxin LuKey Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou, 325035, Zhejiang, People's Republic of China. jxlu313@163.com.
Wenzhou Medical University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial diabetes originates mainly from mutations located in maternally transmitted, mitochondrial tRNA-coding genes. In a genetic screening program of type 2 diabetes conducted with a Chinese Han population, we found one family with suggestive maternally transmitted diabetes. The proband's mitochondrial genome was analyzed using DNA sequencing. Total 42 known nucleoside changes and 1 novel variant were identified, and the entire mitochondrial DNA sequence was assigned to haplogroup M11b. Phylogenetic analysis showed that a homoplasmic mutation, 10003T>C transition, occurred at the highly conserved site in the gene encoding tRNA(Gly). Using a transmitochondrial cybrid cell line harboring this mutation, we observed that the steady-state level of tRNA(Gly) significantly affected and the amount of tRNA(Gly) decreased by 97%, production of reactive oxygen species was enhanced, and mitochondrial membrane potential, mtDNA copy number and cellular oxygen consumption rate were remarkably decreased compared with wild-type cybrid cells. The homoplasmic 10003T>C mutation in the mitochondrial tRNA(Gly) gene suggested to be as a pathogenesis-related mutation which might contribute to the maternal inherited diabetes in the Han Chinese family.

Indexed as

MutationAgedAsian PeopleChinaDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGenome, MitochondrialHaplotypesHumansMaleMembrane Potential, MitochondrialMiddle AgedMitochondriaMitochondrial DiseasesOxygen ConsumptionReactive Oxygen SpeciesRNA, Transfer, Glym.10003T>C mutationMitochondrial diabetesMitochondrial membrane potentialMitochondrial tRNA glycineReactive oxygen species

Identifiers

PMID26134044
OpenAlexW854166115

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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.