Evidence map›Paper›PMID 15888915›Full record

ReviewImmunologic research2005

The proteasome: a central regulator of inflammation and macrophage function.

Nilofer Qureshi, Stefanie N Vogel, Charles Van Way, Christopher J Papasian, Asaf A Qureshi, David C Morrison

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

50 citing papers in PubMed, 91 citations in OpenAlex.

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  10. MiR-19a mediates the negative regulation of the NF-κB pathway in lipopolysaccharide-induced endometritis by targeting TBK1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
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  16. Review
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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

6 authors at 3 institutions in 1 country.

Nilofer QureshiDepartment of Basic Medical Science, School of Medicine, Shock/Trauma Research Center, University of Maryland-Baltimore, Baltimore, MD, USA. qureshin@umkc.edu
Stefanie N Vogel
Charles Van Way
Christopher J Papasian
Asaf A Qureshi
David C Morrison
University of Maryland, Baltimore · USUniversity of Maryland Medical Center · USUniversity of Missouri–Kansas City · US

Funding

DIFFERENTIATIVE SIGNALS FOR MACROPHAGE ACTIVATIONR37AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2000 to 2009
$5.3M
DIFFERENTIATIVE SIGNALS FOR MACROPHANGE ACTIVATIONR01AI018797 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI VOGEL, STEFANIE N. · 1985 to 2014
$3.8M
MECHANISMS INVOLVED IN THE SEPTIC SHOCK SYNDROMER01GM050870 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI QURESHI, NILOFER · 1994 to 2010
$3.4M
Differentiative Signals for Macrophage ActivationR56AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2015 to 2015
$506k
IMMUNOCHEMISTRY OF ENDOTOXIN UNRESPONSIVE C3H/HEJ MICER01AI023447 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MORRISON, DAVID C. · 1986 to 1989
–
IMMUNOCHEMISTRY OF ENDOTOXIN-UNRESPONSIVE C3H-HEJ MICER37AI023447 · NIAID · UNIVERSITY OF MISSOURI KANSAS CITY · PI MORRISON, DAVID C. · 1990 to 1999
–
NIAID NIH HHS AI 18797NIAID NIH HHS AI 23447NIGMS NIH HHS GM 50870NIGMS NIH HHS R01 GM050870
6 · The paper itself

Abstract

Proteasomes, multisubunit complexes that consist of a 20S proteasome and a 19S regulatory complex, are essential for several cellular processes. Our interest in the proteasome complex stems from our observations that a novel photoactivable lipopolysaccharide (LPS) probe binds to specific proteasome subunits, and that LPS enhances the chymotrypsin-like activity of the proteasome to degrade synthetic peptides in vitro. Experiments with proteasome inhibitors have shown that expression of many LPS-inducible genes, including TLR2, is inhibited in macrophages. More important, proteasome inhibitors such as lactacystin can prevent LPS-induced shock in mice. This article focuses on the role of the proteasome in the development of inflammatory processes, which may result in septic shock, hemorrhagic shock, atherosclerosis, and neurodegenerative disorders. Taken collectively, the results suggest a potentially important role of the proteasome in inflammation and other macrophage functions.

Indexed as

AcetylcysteineAgingAnimalsAtherosclerosisCholesterolHumansInflammationLipopolysaccharidesMacrophagesMiceNeurodegenerative DiseasesProteasome Endopeptidase ComplexProteasome InhibitorsShock, HemorrhagicSignal TransductionToll-Like Receptor 2AcetylcysteineCholesterollactacystinLipopolysaccharidesProteasome Endopeptidase ComplexProteasome InhibitorsToll-Like Receptor 2

Identifiers

PMID15888915
OpenAlexW2322598508

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.