Evidence map›Paper›PMID 29061763›Full record

ArticleThe EMBO journal2017

A TNF-p100 pathway subverts noncanonical NF-κB signaling in inflamed secondary lymphoid organs.

Tapas Mukherjee, Budhaditya Chatterjee, Atika Dhar, Sachendra S Bais, Meenakshi Chawla, Payel Roy, Anna George, Vineeta Bal, Satyajit Rath, Soumen Basak

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. RelB upregulates PD-L1 and exacerbates prostate cancer immune evasion.Journal of experimental & clinical cancer research : CR · 2022
    Article
  9. CD169Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. An epithelialProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Substrate complex competition is a regulatory motif that allows NFκB RelA to license but not amplify NFκB RelB.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  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

10 authors at 1 institution in 1 country.

Tapas MukherjeeSystems Immunology Laboratory National Institute of Immunology, New Delhi, India.
Budhaditya ChatterjeeSystems Immunology Laboratory National Institute of Immunology, New Delhi, India.
Atika DharNational Institute of Immunology, New Delhi, India.
Sachendra S BaisSystems Immunology Laboratory National Institute of Immunology, New Delhi, India.
Meenakshi ChawlaSystems Immunology Laboratory National Institute of Immunology, New Delhi, India.
Payel RoySystems Immunology Laboratory National Institute of Immunology, New Delhi, India.
Anna GeorgeNational Institute of Immunology, New Delhi, India.
Vineeta BalNational Institute of Immunology, New Delhi, India.
Satyajit RathNational Institute of Immunology, New Delhi, India.
Soumen BasakSystems Immunology Laboratory National Institute of Immunology, New Delhi, India sobasak@nii.ac.in.ORCID 0000-0002-3586-1279
National Institute of Immunology · IN

Funding

Wellcome TrustWellcome Trust 500094/Z/09/Z
6 · The paper itself

Abstract

Lymphotoxin-beta receptor (LTβR) present on stromal cells engages the noncanonical NF-κB pathway to mediate RelB-dependent expressions of homeostatic chemokines, which direct steady-state ingress of naïve lymphocytes to secondary lymphoid organs (SLOs). In this pathway, NIK promotes partial proteolysis of p100 into p52 that induces nuclear translocation of the RelB NF-κB heterodimers. Microbial infections often deplete homeostatic chemokines; it is thought that infection-inflicted destruction of stromal cells results in the downregulation of these chemokines. Whether inflammation

Indexed as

Adaptive ImmunityAnimalsChemokinesDown-RegulationI-kappa B KinaseInflammation MediatorsLymphangitisLymphoid TissueLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNF-kappaB-Inducing KinaseNF-kappa B p52 SubunitProtein Serine-Threonine KinasesChemokinesChuk protein, mouseI-kappa B KinaseInflammation MediatorsLtbr protein, mouseLymphotoxin beta ReceptorNF-kappa BNF-kappaB-Inducing KinaseNF-kappa B p52 SubunitNfkb2 protein, mouseProtein Serine-Threonine KinasesRelb protein, mouseRNA, MessengerTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3TRAF2 protein, mouseTranscription Factor RelBTumor Necrosis Factor-alphahomeostatic chemokineinhibitionlymphocyte traffickingnoncanonical NF‐kappaBTNF

Identifiers

PMID29061763
PMCPMC5709727
OpenAlexW2766332818

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.