Evidence map›Paper›PMID 22976836›Full record

ArticleCell death and differentiation2013

TAp73 is required for macrophage-mediated innate immunity and the resolution of inflammatory responses.

R Tomasini, V Secq, L Pouyet, A K Thakur, M Wilhelm, J Nigri, S Vasseur, P Berthezene, E Calvo, G Melino and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. TAp73 represses NF-κB-mediated recruitment of tumor-associated macrophages in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Review
  9. TAp73 upregulates IL-1β in cancer cells: Potential biomarker in lung and breast cancer?Biochemical and biophysical research communications · 2017
    Article
  10. How Does p73 Cause Neuronal Defects?Molecular neurobiology · 2016
    Review
  11. Resolution of inflammation: a new therapeutic frontier.Nature reviews. Drug discovery · 2016
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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

12 authors at 5 institutions in 4 countries.

R TomasiniINSERM U1068, CRCM, Stress Cellulaire, 163 Avenue de Luminy, Case 915, Parc de Luminy, 13288 Marseille Cedex 9, France. richard.tomasini@inserm.fr
V Secq
L Pouyet
A K Thakur
M Wilhelm
J Nigri
S Vasseur
P Berthezene
E Calvo
G Melino
T W Mak
J L Iovanna
Inserm · FRIstituti di Ricovero e Cura a Carattere Scientifico · ITKarolinska Institutet · SEUniversité Laval · CAUniversity Health Network · CA

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

The multiple isoforms of p73, a member of the p53 family, share the ability to modulate p53 activities but also have unique properties, leading to a complex and poorly understood functional network. In vivo, p73 isoforms have been implicated in tumor suppression (TAp73(-/-) mice), DNA damage (ΔNp73(-/-) mice) and development (p73(-/-) mice). In this study, we investigated whether TAp73 contributes to innate immunity and septic shock. In response to a lethal lipopolysaccharide (LPS) challenge, TAp73(-/-) mice showed higher blood levels of proinflammatory cytokines and greater mortality than their wild-type littermates. In vitro, TAp73(-/-) macrophages exhibited elevated production of tumor necrosis factor alpha , interleukin-6 and macrophage inflammatory protein-2 as well as prolonged survival, decreased phagocytosis and increased major histocompatibility complex class II expression. Mice depleted of endogenous macrophages and reconstituted with TAp73(-/-) macrophages showed increased sensitivity to LPS challenge. These results suggest that macrophage polarization is altered in the absence of TAp73 such that maintenance of the M1 effector phenotype is prolonged at the expense of the M2 phenotype, thus impairing resolution of the inflammatory response. Our data indicate that TAp73 has a role in macrophage polarization and innate immunity, enhancing the action field of this important regulatory molecule.

Indexed as

Immunity, InnateAnimalsCells, CulturedChemokine CXCL2DNA-Binding ProteinsGene Expression RegulationInterferon-betaInterleukin-6LipopolysaccharidesMacrophagesMaleMiceMice, Inbred BALB CMice, KnockoutNuclear ProteinsPhenotypeChemokine CXCL2DNA-Binding ProteinsInterferon-betaInterleukin-6LipopolysaccharidesNuclear ProteinsProtein IsoformsTrp73 protein, mouseTumor Necrosis Factor-alphaTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID22976836
PMCPMC3554333
OpenAlexW1981450753

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.