Evidence map›Paper›PMID 16283522›Full record

ArticleMolecular and cellular biochemistry2005

Inhibition of core histones acetylation by carcinogenic nickel(II).

Filip Golebiowski, Kazimierz S Kasprzak

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2005. 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
1.1field-weighted citation impact, top 25% 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, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. 10th NTES Conference: Nickel and Arsenic Compounds Alter the Epigenome of Peripheral Blood Mononuclear Cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2015
    Article
  12. Epigenetic dysregulation by nickel through repressive chromatin domain disruption.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Article
  15. The effect of exposure to carcinogenic metals on histone tail modifications and gene expression in human subjects.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2012
    Review
  16. Environmental chemical exposures and human epigenetics.International journal of epidemiology · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Filip GolebiowskiLaboratory of Comparative Carcinogenesis, NCI at Frederick, Frederick, MD, 21702-1201, USA. filip@ncifcrf.gov
Kazimierz S Kasprzak
Genesis Laboratories · US

Funding

MECHANISMS OF TRANSITION METAL-INDUCED CARCINOGENESISZ01BC004582 · NCI · BASIC SCIENCES · PI KASPRZAK, KAZIMIERZ S · 1996 to 2007
$629k
6 · The paper itself

Abstract

Nickel, a well-established human carcinogen, was shown to decrease acetylation of histones H4 and H3 in cultured cells. Such a decrease is expected to suppress gene expression. However, nickel is known to not only suppress but also enhance the expression of many genes. So, perhaps, nickel can alter histone acetylation in a more complex way? In a first step of testing this presumption, we examined acetylation status of histones H2A, H2B, H3 and H4, in human (HAE) and rat (NRK) cells exposed to nickel(II) under various conditions. In both cell lines, acetylation of all four histones was down-regulated by nickel(II) in a concentration- and time-dependent manner. Acetylation of histone H2B was suppressed to greater extent than that of the others, with histone H3 being relatively least affected. The analysis of acetylation status of each of the four lysine sites at the N-terminal tail of histone H2B revealed decreases consistent with those observed in the total acetylation patterns, with the K12 and K20 residues being markedly more affected than K5 and K15 residues. Thus, the decrease in acetylation was to some degree site specific. In NRK cells, the observed uniform down-regulation of histone acetylation was consistent with a marked suppression of global gene transcription measured as [3H]-uridine incorporation into mRNA. However, in HAE cells, global RNA expression was transiently increased (in 24 h) before dropping below control after longer exposure (3 days). In conclusion, the effects of Ni(II) on histone acetylation are inhibitory, with their extent depending on the dose and exposure time. This uniform inhibition, however, is not consistently reflected in global RNA expression that in HAE cells may include both increase and decrease of the expression, clearly indicating the involvement of factors other than histone acetylation. The observed effects may contribute to neoplastic transformation of Ni(II)-exposed cells.

Indexed as

AcetatesAcetylationAnimalsCarcinogensCell LineCell Transformation, NeoplasticDose-Response Relationship, DrugEpithelial CellsGene ExpressionHistonesHumansLysineOrganometallic CompoundsTime FactorsTranscription, GeneticAcetatesCarcinogensHistonesLysinenickel acetateOrganometallic Compounds

Identifiers

PMID16283522
OpenAlexW1965220319

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.