Evidence map›Paper›PMID 19181875›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2009

The role of the ubiquitin proteasome system in ischemia and ischemic tolerance.

Robert Meller

Open access · greenAbstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

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  19. Patterns of ubiquitylation and SUMOylation associated with exposure to anoxia in embryos of the annual killifish Austrofundulus limnaeus.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2014
    Article
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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

1 author at 1 institution in 1 country.

Robert MellerLegacy Clinical Research and Technology Center, Portland, Oregon, USA. rmeller@downeurobiology.org
Legacy Health · US

Funding

CELL EXCITATION IN ISCHEMIC BRAIN INJURYR01NS024728 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIMON, ROGER PANCOAST · 1988 to 2010
$3.5M
MOLECULAR MECHANISMS OF SEIZURE INDUCED BRAIN INJURYR01NS039016 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIMON, ROGER PANCOAST · 1999 to 2009
$2.6M
Protein ubiquitination based neuroprotection for strokeR21NS050669 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI MELLER, ROBERT · 2005 to 2006
$354k
Rapid ischemic tolerance: Ubiquitin-mediated structural reorganizationR21NS054023 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI MELLER, ROBERT · 2006 to 2007
$344k
NINDS NIH HHS NS024728NINDS NIH HHS NS039016NINDS NIH HHS NS050669NINDS NIH HHS NS054023NINDS NIH HHS R01 NS024728NINDS NIH HHS R01 NS039016NINDS NIH HHS R21 NS050669NINDS NIH HHS R21 NS054023
6 · The paper itself

Abstract

Ubiquitin modification targets a protein for rapid degradation by the proteasome. However, polyubiquitination of proteins can result in multiple functions depending on the topology of the ubiquitin chain. Therefore, ubiquitin signaling offers a more complex and versatile biology compared with many other posttranslational modifications. One area of potential for the application of this knowledge is the field of ischemia-induced brain damage, as occurs following a stroke. The ubiquitin proteasome system may exert a dual role on neuronal outcome following ischemia. Harmful ischemia results in an overload of the ubiquitin proteasome system, and blocking the proteasome reduces brain infarction following ischemia. However, the rapid and selective degradation of proteins following brief ischemia results in endogenous protection against ischemia. Therefore, further understanding of the molecular signaling mechanisms that regulate the ubiquitin proteasome system may reveal novel therapeutic targets to reduce brain damage when ischemia is predicted or reduce the activation of the cell death mechanisms and the inflammatory response following stroke. The aim of this review is to discuss some of the recent advances in the understanding of protein ubiquitination and its implications for novel stroke therapies.

Indexed as

Ischemic PreconditioningAnimalsBrainHumansIschemiaModels, BiologicalProteasome Endopeptidase ComplexUbiquitinProteasome Endopeptidase ComplexUbiquitin

Identifiers

PMID19181875
PMCPMC2946222
OpenAlexW2067225359

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.