Evidence map›Paper›PMID 25995453›Full record

ArticleThe Journal of biological chemistry2015

SET7/9 Enzyme Regulates Cytokine-induced Expression of Inducible Nitric-oxide Synthase through Methylation of Lysine 4 at Histone 3 in the Islet β Cell.

Kyoko Fujimaki, Takeshi Ogihara, David L Morris, Hisanobu Oda, Hitoshi Iida, Yoshio Fujitani, Raghavendra G Mirmira, Carmella Evans-Molina, Hirotaka Watada

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence 
and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Article
  7. Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Epigenetics of metabolic syndrome.Physiological genomics · 2018
    Review
  15. Article
  16. SET7/9 inhibits oncogenic activities through regulation of Gli-1 expression in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Article
  18. Article
  19. 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

9 authors at 4 institutions in 4 countries.

Kyoko FujimakiFrom the Department of Metabolism and Endocrinology.
Takeshi OgiharaFrom the Department of Metabolism and Endocrinology, take@juntendo.ac.jp.
David L MorrisMedicine, and.
Hisanobu OdaDepartment of Gastrointestinal and Medical Oncology, National Hospital Organization Kyushu Cancer Center, Fukuoka 811-1395, Japan.
Hitoshi IidaFrom the Department of Metabolism and Endocrinology.
Yoshio FujitaniFrom the Department of Metabolism and Endocrinology, Therapeutic Innovations in Diabetes, and Japan Science and Technology Agency-Core Research for Evolutionary Science and Technology Program, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Raghavendra G MirmiraMedicine, and Departments of Biochemistry and Molecular Biology, Cellular and Integrative Physiology and the Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, and.
Carmella Evans-MolinaMedicine, and Departments of Biochemistry and Molecular Biology, Cellular and Integrative Physiology and the Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, and cevansmo@iu.edu.
Hirotaka WatadaFrom the Department of Metabolism and Endocrinology, Therapeutic Innovations in Diabetes, and Centers for Molecular Diabetology and.
Endocrinology Research Center · RULaboratoire d’immunologie intégrative du cancer · FRJapan Science and Technology Agency · JPNational Hospital Organization Kyushu Cancer Center · JP

Funding

Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Amelia K Linnemann · 2015 to 2026
$17.4M
Mechanisms of Beta Cell Function in Health and DiseaseR01DK093954 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2011 to 2019
$3.5M
Chromatin Cofactors in Islet Development and FunctionR01DK083583 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI MIRMIRA, RAGHAVENDRA G · 2010 to 2013
$1.2M
Function and Regulation of Islet-associated Macrophages in Obesity and DiabetesK01DK100515 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI MORRIS, DAVID L · 2013 to 2016
$437k
Role of CD40 in Obesity-Induced Adipose Tissue Inflammation & Insulin ResistanceF32DK091976 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORRIS, DAVID L · 2011 to 2013
$134k
Regulation of Calcium Homeostasis in the Pancreatic Beta CellI01BX001733 · VA · RLR VA MEDICAL CENTER · PI Carmella Evans-Molina · 2013 to 2026
–
BLRD VA I01 BX001733NIDDK NIH HHS F32 DK091976NIDDK NIH HHS K01 DK100515NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK093954
6 · The paper itself

Abstract

SET7/9 is an enzyme that methylates histone 3 at lysine 4 (H3K4) to maintain euchromatin architecture. Although SET7/9 is enriched in islets and contributes to the transactivation of β cell-specific genes, including Ins1 and Slc2a, SET7/9 has also been reported to bind the p65 subunit of nuclear factor κB in non-β cells and modify its transcriptional activity. Given that inflammation is a central component of β cell dysfunction in Type 1 and Type 2 diabetes, the aim of this study was to elucidate the role of SET7/9 in proinflammatory cytokine signaling in β cells. To induce inflammation, βTC3 insulinoma cells were treated with IL-1β, TNF-α, and IFN-γ. Cytokine treatment led to increased expression of inducible nitric-oxide synthase, which was attenuated by the diminution of SET7/9 using RNA interference. Consistent with previous reports, SET7/9 was co-immunoprecipitated with p65 and underwent cytosolic to nuclear translocation in response to cytokines. ChIP analysis demonstrated augmented H3K4 mono- and dimethylation of the proximal Nos2 promoter with cytokine exposure. SET7/9 was found to occupy this same region, whereas SET7/9 knockdown attenuated cytokine-induced histone methylation of the Nos2 gene. To test this relationship further, islets were isolated from SET7/9-deficient and wild-type mice and treated with IL-1β, TNF-α, and IFN-γ. Cytokine-induced Nos2 expression was reduced in the islets from SET7/9 knock-out mice. Together, our findings suggest that SET7/9 contributes to Nos2 transcription and proinflammatory cytokine signaling in the pancreatic β cell through activating histone modifications.

Indexed as

AnimalsApoptosisHistone-Lysine N-MethyltransferaseHistonesInsulin-Secreting CellsInterferon-gammaInterleukin-1Interleukin-1betaIslets of LangerhansLysineMethylationMiceMice, KnockoutNitric Oxide Synthase Type IIProtein MethyltransferasesTumor Necrosis Factor-alphaHistone-Lysine N-MethyltransferaseHistonesInterferon-gammaInterleukin-1Interleukin-1betaLysineNitric Oxide Synthase Type IINos2 protein, mouseProtein MethyltransferasesSetd7 protein, mouseTumor Necrosis Factor-alphabeta cell (β-cell)histone methylationinflammationisletnitric-oxide synthasep65Set9

Identifiers

PMID25995453
PMCPMC4505414
OpenAlexW1522965187

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.