Evidence map›Paper›PMID 17083329›Full record

ArticleThe Biochemical journal2007

Histone acetyltransferase MOZ acts as a co-activator of Nrf2-MafK and induces tumour marker gene expression during hepatocarcinogenesis.

Kumiko Ohta, Megumi Ohigashi, Ayako Naganawa, Hiromi Ikeda, Masaharu Sakai, Jun-ichi Nishikawa, Masayoshi Imagawa, Shigehiro Osada, Tsutomu Nishihara

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. MafK acceleratesAging · 2022
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  5. Review
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  7. Epigenetic regulation of Keap1-Nrf2 signaling.Free radical biology & medicine · 2015
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Transcriptional regulation of the human ferritin gene by coordinated regulation of Nrf2 and protein arginine methyltransferases PRMT1 and PRMT4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  14. Review
  15. Article
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  19. Article
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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

9 authors at 3 institutions in 1 country.

Kumiko OhtaLaboratory of Environmental Biochemistry, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-Oka, Suita, Osaka 565-0871, Japan.
Megumi Ohigashi
Ayako Naganawa
Hiromi Ikeda
Masaharu Sakai
Jun-ichi Nishikawa
Masayoshi Imagawa
Shigehiro Osada
Tsutomu Nishihara
Osaka University · JPHokkaido University · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HATs (histone acetyltransferases) contribute to the regulation of gene expression, and loss or dysregulation of these activities may link to tumorigenesis. Here, we demonstrate that expression levels of HATs, p300 and CBP [CREB (cAMP-response-element-binding protein)-binding protein] were decreased during chemical hepatocarcinogenesis, whereas expression of MOZ (monocytic leukaemia zinc-finger protein; MYST3)--a member of the MYST [MOZ, Ybf2/Sas3, Sas2 and TIP60 (Tat-interacting protein, 60 kDa)] acetyltransferase family--was induced. Although the MOZ gene frequently is rearranged in leukaemia, we were unable to detect MOZ rearrangement in livers with hyperplastic nodules. We examined the effect of MOZ on hepatocarcinogenic-specific gene expression. GSTP (glutathione S-transferase placental form) is a Phase II detoxification enzyme and a well-known tumour marker that is specifically elevated during hepatocarcinogenesis. GSTP gene activation is regulated mainly by the GPE1 (GSTP enhancer 1) enhancer element, which is recognized by the Nrf2 (nuclear factor-erythroid 2 p45 subunit-related factor 2)-MafK heterodimer. We found that MOZ enhances GSTP promoter activity through GPE1 and acts as a co-activator of the Nrf2-MafK heterodimer. Further, exogenous MOZ induced GSTP expression in rat hepatoma H4IIE cells. These results suggest that during early hepatocarcinogenesis, aberrantly expressed MOZ may induce GSTP expression through the Nrf2-mediated pathway.

Indexed as

Biomarkers, TumorGene ExpressionAnimalsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCell Transformation, NeoplasticDimerizationGlutathione S-Transferase piHistone AcetyltransferasesLiver NeoplasmsMafK Transcription FactorMiceNF-E2-Related Factor 2Promoter Regions, GeneticProtein BindingRatsBiomarkers, TumorCCAAT-Enhancer-Binding ProteinsGlutathione S-Transferase piHistone AcetyltransferasesKat6a protein, ratMafK Transcription FactorNF-E2-Related Factor 2

Identifiers

PMID17083329
PMCPMC1863558
OpenAlexW1978873589

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.