Evidence map›Paper›PMID 22431725›Full record

Trial reportThe Journal of biological chemistry2012

Profiles of epigenetic histone post-translational modifications at type 1 diabetes susceptible genes.

Feng Miao, Zhuo Chen, Lingxiao Zhang, Zheng Liu, Xiwei Wu, Yate-Ching Yuan, Rama Natarajan

Open access · hybridAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
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  15. Review
  16. An update on epigenetic regulation in autoimmune diseases.Journal of translational autoimmunity · 2022
    Article
  17. Review
  18. Diabetes: discovery of insulin, genetic, epigenetic and viral infection mediated regulation.The Nucleus : an international journal of cytology and allied topics · 2022
    Review
  19. Basics of Epigenetics and Role of Epigenetics in Diabetic Complications.Journal of pharmacy & bioallied sciences · 2021
    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

7 authors at 1 institution in 1 country.

Feng MiaoDepartment of Diabetes and Bioinformatics Core, Beckman Research Institute of City of Hope, Duarte, California 91010, USA.
Zhuo Chen
Lingxiao Zhang
Zheng Liu
Xiwei Wu
Yate-Ching Yuan
Rama Natarajan
City of Hope · US

Funding

ZOPOLRESTAT IN NORMOTENSIVE, TYPE 1 DIA WITH INCIPIENT NEPHROPATHYM01RR000043 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZAIA, JOHN A · 1985 to 2010
$76.4M
Inflammatory Gene Transcription In Diabetic ConditionsR01DK065073 · NIDDK · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI NATARAJAN, RAMA · 2003 to 2021
$7.9M
Nuclear Mechanisms of VSMC Gene Regulation and Cellular Interactions in DiabetesR01HL087864 · NHLBI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NATARAJAN, RAMA · 2008 to 2012
$2.1M
NCRR NIH HHS M01 RR000043NCRR NIH HHS M01RR00043NHLBI NIH HHS R01 HL087864NIDDK NIH HHS R01 DK065073
6 · The paper itself

Abstract

Both genetic and environmental factors are implicated in type 1 diabetes (T1D). Because environmental factors can trigger epigenetic changes, we hypothesized that variations in histone post-translational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy nondiabetic controls, and explored their connections to T1D. We used the chromatin immunoprecipitation-linked to microarray approach to profile key histone PTMs, including H3-lysine 4 trimethylation (H3K4me3), H3K27me3, H3K9me3, H3K9 acetylation (H3K9Ac), and H4K16Ac at genes within the T1D susceptible loci in lymphocytes, and H3K4me3, H3K9me2, H3K9Ac, and H4K16Ac at the insulin-dependent diabetes mellitus 1 region in monocytes of T1D patients and healthy controls separately. We screened for potential variations in histone PTMs using computational methods to compare datasets from T1D and controls. Interestingly, we observed marked variations in H3K9Ac levels at the upstream regions of HLA-DRB1 and HLA-DQB1 within the insulin-dependent diabetes mellitus 1 locus in T1D monocytes relative to controls. Additional experiments with THP-1 monocytes demonstrated increased expression of HLA-DRB1 and HLA-DQB1 in response to interferon-γ and TNF-α treatment that were accompanied by changes in H3K9Ac at the same promoter regions as that seen in the patient monocytes. These results suggest that the H3K9Ac status of HLA-DRB1 and HLA-DQB1, two genes highly associated with T1D, may be relevant to their regulation and transcriptional response toward external stimuli. Thus, the promoter/enhancer architecture and chromatin status of key susceptible loci could be important determinants in their functional association to T1D susceptibility.

Indexed as

Epigenesis, GeneticGenetic Predisposition to DiseaseProtein Processing, Post-TranslationalDiabetes Mellitus, Type 1FemaleGenetic LociHistonesHLA-DQ beta-ChainsHLA-DRB1 ChainsHumansMaleHistonesHLA-DQB1 antigenHLA-DQ beta-ChainsHLA-DRB1 Chains

Identifiers

PMID22431725
PMCPMC3351309
OpenAlexW2025328449

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.