Evidence map›Paper›PMID 23460747›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

An extraribosomal function of ribosomal protein L13a in macrophages resolves inflammation.

Darshana Poddar, Abhijit Basu, William M Baldwin, Roman V Kondratov, Sailen Barik, Barsanjit Mazumder

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 65 citations in OpenAlex.

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  13. Loss of function of ribosomal protein L13a blocks blastocyst formation and reveals a potential nuclear role in gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  14. Specialized Ribosomes in Health and Disease.International journal of molecular sciences · 2023
    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 2 institutions in 1 country.

Darshana PoddarDepartment of Biological, Geological, and Environmental Sciences, Center for Gene Regulation in Health and Disease, Cleveland State University, Cleveland, OH 44115, USA.
Abhijit Basu
William M Baldwin
Roman V Kondratov
Sailen Barik
Barsanjit Mazumder
Cleveland State University · USCleveland Clinic Lerner College of Medicine · US

Funding

Surgery CoreP01AI087586 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI VALUJSKIKH, ANNA · 2010 to 2019
$17.2M
Diversity Supplement for Circadian Clock and Dietary RestrictionR01AG039547 · NIA · CLEVELAND STATE UNIVERSITY · PI Roman V Kondratov · 2011 to 2026
$5.5M
Translational Silencing in Monocytes: Role of L13aR01HL079164 · NHLBI · CLEVELAND STATE UNIVERSITY · PI MAZUMDER, BARSANJIT · 2005 to 2019
$4.5M
Mechanisms of RNA virus-host interactionR01AI059267 · NIAID · UNIVERSITY OF SOUTH ALABAMA · PI BARIK, SAILEN · 2005 to 2009
$1.2M
NHLBI NIH HHS NIH HL79164NHLBI NIH HHS R01 HL079164NIAID NIH HHS AI 059267NIAID NIH HHS P01 AI087586NIAID NIH HHS P01AI087586NIAID NIH HHS R01 AI059267NIA NIH HHS AG 033604
6 · The paper itself

Abstract

Inflammation is an obligatory attempt of the immune system to protect the host from infections. However, unregulated synthesis of proinflammatory products can have detrimental effects. Although mechanisms that lead to inflammation are well appreciated, those that restrain it are not adequately understood. Creating macrophage-specific L13a-knockout mice, we report that depletion of ribosomal protein L13a abrogates the endogenous translation control of several chemokines in macrophages. Upon LPS-induced endotoxemia, these animals displayed symptoms of severe inflammation caused by widespread infiltration of macrophages in major organs causing tissue injury and reduced survival rates. Macrophages from these knockout animals show unregulated expression of several chemokines (e.g., CXCL13, CCL22, CCL8, and CCR3). These macrophages failed to show L13a-dependent RNA binding complex formation on target mRNAs. In addition, increased polyribosomal abundance of these mRNAs shows a defect in translation control in the macrophages. Thus, to our knowledge, our studies provide the first evidence of an essential extraribosomal function of ribosomal protein L13a in resolving physiological inflammation in a mammalian host.

Indexed as

AnimalsEndotoxemiaEndotoxinsFemaleGene DeletionGenetic Predisposition to DiseaseHomozygoteInflammationLeukocytesMacrophagesMaleMiceMice, KnockoutMyeloid CellsOrgan SpecificityPeritoneumEndotoxinsRibosomal ProteinsRpl13a protein, mouse

Identifiers

PMID23460747
PMCPMC3608820
OpenAlexW2129084302

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.