Evidence map›Paper›PMID 26853469›Full record

ArticleOncogene2016

A RelA(p65) Thr505 phospho-site mutation reveals an important mechanism regulating NF-κB-dependent liver regeneration and cancer.

A Moles, J A Butterworth, A Sanchez, J E Hunter, J Leslie, H Sellier, D Tiniakos, S J Cockell, D A Mann, F Oakley and 1 more

Abstract read
In one paragraph

Article in Oncogene, 2016. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Article
  4. World journal of gastroenterology · 2025
    Article
  5. Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Benzophenones fromMolecules (Basel, Switzerland) · 2019
    Article
  17. Review
  18. Review
  19. Role of the NFκB-signaling pathway in cancer.OncoTargets and therapy · 2018
    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

11 authors.

A MolesInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
J A ButterworthInstitute for Cell and Molecular Biosciences (ICaMB), Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
A SanchezInstitute for Cell and Molecular Biosciences (ICaMB), Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
J E HunterInstitute for Cell and Molecular Biosciences (ICaMB), Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
J LeslieInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
H SellierInstitute for Cell and Molecular Biosciences (ICaMB), Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
D TiniakosInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
S J CockellBioinformatics Support Unit, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
D A MannInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
F OakleyInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
N D PerkinsInstitute for Cell and Molecular Biosciences (ICaMB), Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.

Funding

Cancer Research UK 12750Cancer Research UK 22095Cancer Research UK A12750Medical Research Council G0900535Medical Research Council MR/K001949/1National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K000748/1Wellcome Trust 094409
6 · The paper itself

Abstract

Post-translational modifications of nuclear factor (NF)-κB subunits provide a mechanism to differentially regulate their activity in response to the many stimuli that induce this pathway. However, the physiological significance of these modifications is largely unknown, and it remains unclear if these have a critical role in the normal and pathological functions of NF-κB in vivo. Among these, phosphorylation of the RelA(p65) Thr505 residue has been described as an important regulator of NF-κB activity in cell lines, but its physiological significance was not known. Therefore, to learn more about the role of this pathway in vivo, we generated a knockin mouse with a RelA T505A mutation. Unlike RelA knockout mice, the RelA T505A mice develop normally but exhibit aberrant hepatocyte proliferation following liver partial hepatectomy or damage resulting from carbon tetrachloride (CCl4) treatment. Consistent with these effects, RelA T505A mice exhibit earlier onset of cancer in the N-nitrosodiethylamine model of hepatocellular carcinoma. These data reveal a critical pathway controlling NF-κB function in the liver that acts to suppress the tumour-promoting activities of RelA.

Indexed as

AnimalsApoptosisCarbon TetrachlorideCell ProliferationGene Knock-In TechniquesHepatocytesHumansLiver NeoplasmsLiver RegenerationMiceMice, KnockoutMutationNF-kappa BPhosphorylationTranscription Factor RelACarbon TetrachlorideNF-kappa BRela protein, mouseTranscription Factor RelA

Identifiers

PMID26853469
PMCPMC4862573

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Registered trials

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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.