Evidence map›Paper›PMID 16862178›Full record

ArticleOncogene2007

NF-kappaB activation by combinations of NEMO SUMOylation and ATM activation stresses in the absence of DNA damage.

S M Wuerzberger-Davis, Y Nakamura, B J Seufzer, S Miyamoto

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Sub-cellular localization specific SUMOylation in the heart.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  15. Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017
    Review
  16. SUMO and the robustness of cancer.Nature reviews. Cancer · 2017
    Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

S M Wuerzberger-DavisCancer Biology Program, University of Wisconsin-Madison, Madison, WI 53706, USA.
Y Nakamura
B J Seufzer
S Miyamoto
University of Wisconsin–Madison · US

Funding

Regulation of NEMO modifications in radiation-induced NF-kB signalingR01CA077474 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MIYAMOTO, SHIGEKI · 2000 to 2014
$4.0M
MECHANISMS OF CONSTITUTIVE NF KB ACTIVITYR01CA081065 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MIYAMOTO, SHIGEKI · 1999 to 2007
$2.5M
NCI NIH HHS R01-CA77474NCI NIH HHS R01-CA81065
6 · The paper itself

Abstract

The inactive transcription factor NF-kappaB is localized in the cytoplasm and rapidly responds to a variety of extracellular factors and intracellular stress conditions to initiate multiple cellular responses. While the knowledge regarding NF-kappaB signaling pathways initiated by extracellular ligands is rapidly expanding, the mechanisms of activation by intracellular stress conditions are not well understood. We recently described a critical role for a small ubiquitin-like modifier (SUMO) modification of NF-kappaB essential modulator (NEMO), the regulatory subunit of the IkappaB kinase, in response to certain genotoxic stress conditions. One important unanswered question is whether the role of this modification is limited to the genotoxic agents or some other signaling pathways also employ SUMOylation of NEMO to regulate NF-kappaB activation. Here, we report that a variety of other stress conditions, including oxidative stress, ethanol exposure, heat shock and electric shock, also induce NEMO SUMOylation, thus demonstrating that DNA damage per se is not necessary for this NEMO modification to occur. Moreover, combinations of certain SUMO stress and ATM (ataxia telangiectasia mutated) activation conditions lead to NF-kappaB activation without inducing DNA damage. Our study helps to conceptualize how individual or a combination of different stress conditions may funnel into this previously unappreciated signal transduction mechanism to regulate the activity of the ubiquitous NF-kappaB transcription factor.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsBlotting, WesternCell Cycle ProteinsCytoplasmDNA-Binding ProteinsElectric StimulationEmbryo, MammalianEthanolFibroblastsHeat-Shock ResponseIntracellular Signaling Peptides and ProteinsKidneyLeukemia-Lymphoma, Adult T-CellMiceAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsEthanolIntracellular Signaling Peptides and ProteinsNEMO protein, mouseNF-kappa BProtein Serine-Threonine KinasesSUMO-1 ProteinTumor Suppressor ProteinsUbiquitin

Identifiers

PMID16862178
OpenAlexW1992197155

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.