Evidence map›Paper›PMID 18818687›Full record

ReviewKidney international2009

Epigenetics and the control of epithelial sodium channel expression in collecting duct.

Dongyu Zhang, Zhi-yuan Yu, Pedro Cruz, Qun Kong, Shiyu Li, Bruce C Kone

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023
    Review
  3. Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023
    Review
  4. Review
  5. Article
  6. Epigenetic modification: a regulatory mechanism in essential hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Review
  7. Review
  8. Epigenetic Mechanisms and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis.International journal of molecular sciences · 2016
    Review
  14. Review
  15. Review
  16. Review
  17. Environmental origins of hypertension: phylogeny, ontogeny and epigenetics.Hypertension research : official journal of the Japanese Society of Hypertension · 2015
    Review
  18. Review
  19. Histone lysine methylation in diabetic nephropathy.Journal of diabetes research · 2014
    Review
  20. Epigenomics of hypertension.Seminars in nephrology · 2013
    Review
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

6 authors at 1 institution in 1 country.

Dongyu ZhangDivision of Nephrology, Hypertension and Renal Transplantation, University of Florida College of Medicine, Gainesville, Florida 32610, USA.
Zhi-yuan Yu
Pedro Cruz
Qun Kong
Shiyu Li
Bruce C Kone
University of Florida · US

Funding

Regulation of ENaC TranscriptionR01DK075065 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KONE, BRUCE C. · 2006 to 2013
$2.5M
NIDDK NIH HHS R01 DK075065
6 · The paper itself

Abstract

In eukaryotic nuclei, genomic DNA is compacted with histone and nonhistone proteins into a dynamic polymer termed chromatin. Reorganization of chromatin structure through histone modifications, the action of chromatin factors, or DNA methylation, can profoundly change gene expression. These epigenetic modifications allow heritable and potentially reversible changes in gene functioning to occur without altering the DNA sequence, thus extending the information potential of the genetic code. This review provides an introduction to epigenetic concepts for renal investigators and an overview of our work detailing an epigenetic pathway for aldosterone signaling and the control of epithelial Na(+) channel-alpha (ENaCalpha) subunit gene expression in the collecting duct. This new pathway involves a nuclear repressor complex, consisting of histone H3 Lys-79 methyltransferase disruptor of telomeric silencing-1a (Dot1a), ALL1 fused gene from chromosome 9 (Af9), a sequence-specific DNA-binding protein that binds the ENaCalpha promoter, and potentially other nuclear proteins. This complex regulates targeted histone H3 Lys-79 methylation of chromatin associated with the ENaCalpha promoter, thereby suppressing its transcriptional activity. Aldosterone disrupts the Dot1a-Af9 interaction by serum- and glucocorticoid-induced kinase-1 phosphorylation of Af9, and inhibits Dot1a and Af9 expression, resulting in histone H3 Lys-79 hypomethylation at specific subregions, and derepression of the ENaCalpha promoter. The Dot1a-Af9 pathway may also be involved in the control of genes implicated in renal fibrosis and hypertension.

Indexed as

Epigenesis, GeneticAldosteroneAnimalsEpithelial Sodium ChannelsGene Expression RegulationHistonesKidney Tubules, CollectingMiceSignal TransductionAldosteroneEpithelial Sodium ChannelsHistones

Identifiers

PMID18818687
PMCPMC2683399
OpenAlexW1974902695

What OpenQuestion holds

Textmetadata
LicenceTDM
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.