Evidence map›Paper›PMID 11416149›Full record

ArticleMolecular and cellular biology2001

Postrepression activation of NF-kappaB requires the amino-terminal nuclear export signal specific to IkappaBalpha.

T T Huang, S Miyamoto

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.0field-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

43 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. NF-κB and Its Regulators During Pregnancy.Frontiers in immunology · 2021
    Review
  7. Article
  8. Article
  9. Post-translational Modifications of IκBα: The State of the Art.Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Anatomy of a negative feedback loop: the case of IκBα.Journal of the Royal Society, Interface · 2015
    Article
  15. Article
  16. IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.American journal of respiratory cell and molecular biology · 2014
    Article
  17. Article
  18. Article
  19. Molecular basis of NF-κB signaling.Annual review of biophysics · 2013
    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

2 authors at 1 institution in 1 country.

T T HuangProgram in Molecular and Cellular Pharmacology, Department of Pharmacology, University of Wisconsin-Madison, Madison, Wisconsin 53706-1532, USA.
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
NCI NIH HHS R01 CA077474NCI NIH HHS R01 CA77474
6 · The paper itself

Abstract

One of the most prominent NF-kappaB target genes in mammalian cells is the gene encoding one of its inhibitor proteins, IkappaBalpha. The increased synthesis of IkappaBalpha leads to postinduction repression of nuclear NF-kappaB activity. However, it is unknown why IkappaBalpha, among multiple IkappaB family members, is involved in this process and what significance this feedback regulation has beyond terminating NF-kappaB activity. Herein, we report an important IkappaBalpha-specific function dictated by its amino-terminal nuclear export sequence (N-NES). The IkappaBalpha N-NES is necessary for the postinduction export of nuclear NF-kappaB, which is a critical event in reestablishing a permissive condition for NF-kappaB to be rapidly reactivated. We show that although IkappaBalpha and another IkappaB member, IkappaBbeta, can enter the nucleus and repress NF-kappaB DNA-binding activity during the postinduction phase, only IkappaBalpha allows the efficient export of nuclear NF-kappaB. Moreover, swapping the N-terminal region of IkappaBbeta for the corresponding IkappaBalpha sequence is sufficient for the IkappaB chimera protein to export NF-kappaB similarly to IkappaBalpha during the postinduction state. Our findings provide a mechanistic explanation of why IkappaBalpha but not other IkappaB members is crucial for postrepression activation of NF-kappaB. We propose that this IkappaBalpha-specific function is important for certain physiological and pathological conditions where NF-kappaB needs to be rapidly reactivated.

Indexed as

I-kappa B ProteinsActive Transport, Cell NucleusAnimalsCell LineCell NucleusChlorocebus aethiopsCOS CellsDNA-Binding ProteinsFatty Acids, UnsaturatedHumansNF-kappa BNF-KappaB Inhibitor alphaDNA-Binding ProteinsFatty Acids, UnsaturatedI kappa B beta proteinI-kappa B Proteinsleptomycin BNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, human

Identifiers

PMID11416149
PMCPMC87155
OpenAlexW2153377330

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.