Evidence map›Paper›PMID 11286378›Full record

ArticleJournal of inherited metabolic disease2001

Sequence variations in the NDUFA1 gene encoding a subunit of complex I of the respiratory chain.

I Wittig, P Augstein, G K Brown, T Fujii, A Rötig, P Rustin, A Munnich, P Seibel, D Thorburn, B Wissinger and 5 more

Abstract read
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Article in Journal of inherited metabolic disease, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

0 citing papers in PubMed, 13 citations in OpenAlex.

No citing paper in PubMed yet.

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 12 institutions in 8 countries.

I WittigInstitute of Human Genetics, Greifswald, Germany.
P Augstein
G K Brown
T Fujii
A Rötig
P Rustin
A Munnich
P Seibel
D Thorburn
B Wissinger
K Tamboom
A Metspalu
E Lamantea
M Zeviani
M S Wehnert
Institut Necker Enfants Malades · FREuropean Institute of Oncology · ITCentre for Human Genetics · GBEstonian Biocentre · EEInstitute for Diabetes Gerhardt Katsch · DEInstitute of Human Genetics · PLLeibniz Institute for Neurobiology · DEMurdoch Children's Research Institute · AUShiga Medical Center for Children · JPSTZ eyetrial · DEUniversität Greifswald · DEUniversity of Tartu · EE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NDUFA1 is one of the 36 nuclear genes encoding subunits of the mitochondrial complex I involved in the respiratory chain. The human NDUFA1 has been cloned, completely sequenced and mapped to Xq24. In the present study, we searched for sequence variations in NDUFA1 as causative defects in complex I deficiency using genomic DNA of 152 patients with various clinical phenotypes. The patient sample consisted of 54 patients (46 male and 8 female) with Leber heriditary optic neuropathy (LHON) from 48 unrelated families from Germany and 98 patients (72 male and 26 female) with biochemically proven complex I deficiency including Leigh syndrome. Patient DNA was used to amplify all three exons, including the exon/intron boundaries and the promoter region of NDUFA1 for heteroduplex analysis and direct sequencing. In the 152 patients tested, no mutation was found that could be related to any of the disease phenotypes included. However, three single-nucleotide polymorphisms (SNPs) located in the promoter region (SNP G/C at nt -71 and SNP T/C at nt -189) and in intron 1 (SNP T/G nt 1454) were discovered. Allele frequencies of the SNPs were estimated in a German and Estonian control population and compared to complex I-deficient patients. There was no significant difference between the control population, the LHON patients, or the severely affected patients with complex I deficiency, excluding an association of the polymorphisms with the diseases. Our results suggest that mutations in NDUFA1 do not cause the gender difference observed in clinically severe and complex phenotypes with complex I deficiency.

Indexed as

AllelesDNA Mutational AnalysisElectron TransportElectron Transport Complex IFemaleGene FrequencyGenetic VariationHumansLeigh DiseaseMaleMembrane ProteinsNADH DehydrogenaseNADH, NADPH OxidoreductasesNucleic Acid HeteroduplexesOptic Atrophies, HereditaryPolymorphism, Single NucleotideElectron Transport Complex IMembrane ProteinsNADH DehydrogenaseNADH, NADPH OxidoreductasesNDUFA1 protein, humanNdufa1 protein, mammalianNucleic Acid Heteroduplexes

Identifiers

PMID11286378
OpenAlexW2599006540

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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.