Evidence map›Paper›PMID 37250100›Full record

ArticleBBA advances2023

Novel dicarbonyl metabolic pathway via mitochondrial ES1 possessing glyoxalase III activity.

Ginga Ito, Yota Tatara, Ken Itoh, Miwa Yamada, Tetsuro Yamashita, Kimitoshi Sakamoto, Takayuki Nozaki, Kinji Ishida, Yui Wake, Takehito Kaneko and 4 more

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

Article in BBA advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Glyoxalase activities of Parkinson's disease relevant protein DJ-1/PARK7: Past discoveries and future perspectives.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026
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  2. Review
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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

14 authors at 3 institutions in 1 country.

Ginga ItoDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Yota TataraDepartment of Stress Response Science, Center for Advanced Medical Research, Hirosaki University Graduate School of Medicine, 5 Zaifuchou, Hirosaki, Aomori 036-8562, Japan.
Ken ItohDepartment of Stress Response Science, Center for Advanced Medical Research, Hirosaki University Graduate School of Medicine, 5 Zaifuchou, Hirosaki, Aomori 036-8562, Japan.
Miwa YamadaDepartment of Biological Chemistry, Faculty of Agriculture, Iwate University, 3-18-8 Ueda, Morioka, Iwate 020-8550, Japan.
Tetsuro YamashitaDepartment of Biological Chemistry, Faculty of Agriculture, Iwate University, 3-18-8 Ueda, Morioka, Iwate 020-8550, Japan.
Kimitoshi SakamotoDepartment of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki, Aomori 036-8561, Japan.
Takayuki NozakiTechnical Support Center for Life Science Research, Iwate Medical University, 1-1-1 Idaidori, Yahaba, Iwate 028-3694, Japan.
Kinji IshidaTechnical Support Center for Life Science Research, Iwate Medical University, 1-1-1 Idaidori, Yahaba, Iwate 028-3694, Japan.
Yui WakeDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Takehito KanekoDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Tomokazu FukudaDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Eriko SuganoDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Hiroshi TomitaDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Taku OzakiDepartment of Biological Science, Graduate School of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan.
Iwate University · JPHirosaki University · JPIwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycation, caused by reactive dicarbonyls, plays a role in various diseases by forming advanced glycation end products. In live cells, reactive dicarbonyls such as glyoxal (GO) and methylglyoxal (MGO) are produced during cell metabolism, and these should be removed consistently. However, the dicarbonyl metabolic system in the mitochondria remains unclear. It has been speculated that the mammalian mitochondrial protein ES1 is a homolog of bacterial elbB possessing glyoxalase III (GLO3) activity. Therefore, in this study, to investigate ES1 functions and GLO3 activity, we generated

Indexed as

ES1GlyoxalaseMethylglyoxal degradationMitochondriaReactive dicarbonyl

Identifiers

PMID37250100
PMCPMC10209487
OpenAlexW4376645302

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.