Evidence map›Paper›PMID 24569813›Full record

ArticleStroke2014

Small ubiquitin-like modifier 3-modified proteome regulated by brain ischemia in novel small ubiquitin-like modifier transgenic mice: putative protective proteins/pathways.

Wei Yang, Huaxin Sheng, J Will Thompson, Shengli Zhao, Liangli Wang, Pei Miao, Xiaozhi Liu, M Arthur Moseley, Wulf Paschen

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  5. Article
  6. SUMOtherapeutics for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
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  13. Review
  14. SUMOylation as a Therapeutic Target for Myocardial Infarction.Frontiers in cardiovascular medicine · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Small ubiquitin-like modifier 2 (SUMO2) is critical for memory processes in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  19. Review
  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

9 authors at 1 institution in 1 country.

Wei YangFrom the Department of Anesthesiology (W.Y., H.S., L.W., P.M., X.L., W.P.), Proteomics Core Facility (J.W.T., M.A.M.), and Department of Neurobiology (S.Z.), Duke University Medical Center, Durham, NC; and Department of Neurosurgery, The Fifth Central Hospital of Tianjin, Tianjin, China (X.L.).
Huaxin Sheng
J Will Thompson
Shengli Zhao
Liangli Wang
Pei Miao
Xiaozhi Liu
M Arthur Moseley
Wulf Paschen
Fifth Tianjin Central Hospital · CN

Funding

Role of SUMO Conjugation in Ischemia: Significance, Mechanisms and PathwaysR01NS081299 · NINDS · DUKE UNIVERSITY · PI PASCHEN, WULF · 2012 to 2016
$1.7M
SUMO Conjugation and Deep Hypothermia-Induced Organ ProtectionR01HL095552 · NHLBI · DUKE UNIVERSITY · PI PASCHEN, WULF · 2010 to 2012
$1.2M
NHLBI NIH HHS HL095552NHLBI NIH HHS R01 HL095552NINDS NIH HHS NS081299NINDS NIH HHS R01 NS081299
6 · The paper itself

Abstract

background and purposeSmall ubiquitin-like modifier (SUMO) conjugation is a post-translational modification associated with many human diseases. Characterization of the SUMO-modified proteome is pivotal to define the mechanistic link between SUMO conjugation and such diseases. This is particularly evident for SUMO2/3 conjugation, which is massively activated after brain ischemia/stroke, and is believed to be a protective response. The purpose of this study was to perform a comprehensive analysis of the SUMO3-modified proteome regulated by brain ischemia using a novel SUMO transgenic mouse.

methodsTo enable SUMO proteomics analysis in vivo, we generated transgenic mice conditionally expressing tagged SUMO1-3 paralogues. Transgenic mice were subjected to 10 minutes forebrain ischemia and 1 hour of reperfusion. SUMO3-conjugated proteins were enriched by anti-FLAG affinity purification and analyzed by liquid chromatography-tandem mass spectrometry.

resultsCharacterization of SUMO transgenic mice demonstrated that all 3 tagged SUMO paralogues were functionally active, and expression of exogenous SUMOs did not modify the endogenous SUMOylation machinery. Proteomics analysis identified 112 putative SUMO3 substrates of which 91 candidates were more abundant in the ischemia group than the sham group. Data analysis revealed processes/pathways with putative neuroprotective functions, including glucocorticoid receptor signaling, RNA processing, and SUMOylation-dependent ubiquitin conjugation.

conclusionsThe identified proteins/pathways modulated by SUMOylation could be the key to understand the mechanisms linking SUMOylation to neuroprotection, and thus provide new promising targets for therapeutic interventions. The new transgenic mouse will be an invaluable platform for analyzing the SUMO-modified proteome in models of human disorders and thereby help to mechanistically link SUMOylation to the pathological processes.

Indexed as

AnimalsBrain IschemiaIschemic Attack, TransientMass SpectrometryMiceMice, TransgenicProteomeProteomicsRNA Processing, Post-TranscriptionalSmall Ubiquitin-Related Modifier ProteinsStrokeSUMO-1 ProteinUbiquitinsProteomeSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinSUMO2 protein, mouseSumo3 protein, mouseUbiquitinsbrain ischemiaproteomicsSUMO proteinstransgenic mice

Identifiers

PMID24569813
PMCPMC3966925
OpenAlexW2095270739

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.