Evidence map›Paper›PMID 21389784›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Deoxyhypusine synthase haploinsufficiency attenuates acute cytokine signaling.

Andrew T Templin, Bernhard Maier, Yurika Nishiki, Sarah A Tersey, Raghavendra G Mirmira

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05594563 (TArgeting Type 1 Diabetes Using POLyamines), which is not on this map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 26% 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.

NCT05594563 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

TArgeting Type 1 Diabetes Using POLyamines (TADPOL): A Randomized, Double-Masked, Placebo-Controlled Phase 2 Study to Evaluate the Efficacy and Safety of Difluoromethylornithine (DFMO) to Preserve Insulin Production in Type 1 Diabetes

TypeinterventionalSponsorEmily K. SimsRan2023 to 2027Enrolled74ConditionsType 1 DiabetesArmsDFMO, Placebo
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The hypusine pathway inFrontiers in cellular and infection microbiology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Deoxyhypusine synthase, an essential enzyme for hypusine biosynthesis, is required for proper exocrine pancreas development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

5 authors at 2 institutions in 1 country.

Andrew T TemplinDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN USA.
Bernhard Maier
Yurika Nishiki
Sarah A Tersey
Raghavendra G Mirmira
Indiana University School of MedicineIndianapolis Zoo · US

Funding

Transcriptional Mechanisms Governing Beta Cell DifferentiationR01DK060581 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Raghavendra G Mirmira · 2002 to 2026
$8.5M
NIDDK NIH HHS R01 DK060581NIDDK NIH HHS R01 DK60581
6 · The paper itself

Abstract

Deoxyhypusine synthase (DHS) catalyzes the post-translational formation of the amino acid hypusine. Hypusine is unique to the eukaryotic translational initiation factor 5A (eIF5A), and is required for its functions in mRNA shuttling, translational elongation, and stress granule formation. In recent studies, we showed that DHS promotes cytokine and ER stress signaling in the islet β cell and thereby contributes to its dysfunction in the setting of diabetes mellitus. Here, we review the evidence supporting a role for DHS (and hypusinated eIF5A) in cellular stress responses, and provide new data on the phenotype of DHS knockout mice. We show that homozygous knockout mice are embryonic lethal, but heterozygous knockout mice appear normal with no evidence of growth or metabolic deficiencies. Mouse embryonic fibroblasts from heterozygous knockout mice attenuate acute cytokine signaling, as evidenced by reduced production of inducible nitric oxide synthase, but show no statistically significant defects in proliferation or cell cycle progression. Our data are discussed with respect to the utility of sub-maximal inhibition of DHS in the setting of inflammatory states, such as diabetes mellitus.

Indexed as

PhenotypeAnimalsCytokinesDiabetes Mellitus, Type 2Eukaryotic Translation Initiation Factor 5AFibroblastsHaploinsufficiencyInsulin-Secreting CellsMiceMice, KnockoutNitric Oxide Synthase Type IIOxidoreductases Acting on CH-NH Group DonorsPeptide Initiation FactorsRNA-Binding ProteinsSignal TransductionCytokinesdeoxyhypusine synthaseEukaryotic Translation Initiation Factor 5ANitric Oxide Synthase Type IIOxidoreductases Acting on CH-NH Group DonorsPeptide Initiation FactorsRNA-Binding Proteins

Identifiers

PMID21389784
PMCPMC3100881
OpenAlexW2094330276

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.