Evidence map›Paper›PMID 15951441›Full record

ArticleThe Journal of biological chemistry2005

NIBP, a novel NIK and IKK(beta)-binding protein that enhances NF-(kappa)B activation.

Wen-Hui Hu, Julie S Pendergast, Xian-Ming Mo, Roberta Brambilla, Valerie Bracchi-Ricard, Fang Li, Winston M Walters, Bas Blits, Li He, Sandra M Schaal and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.5field-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

73 citing papers in PubMed, 122 citations in OpenAlex.

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  19. A novel homozygous variant inJournal of medical genetics · 2021
    Article
  20. Review

13 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Wen-Hui HuThe Miami Project to Cure Paralysis, Department of Neurological Surgery, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Julie S Pendergast
Xian-Ming Mo
Roberta Brambilla
Valerie Bracchi-Ricard
Fang Li
Winston M Walters
Bas Blits
Li He
Sandra M Schaal
John R Bethea
University of Miami · USNeurological Surgery · USSichuan University · CN

Funding

IS INHIBITING SPINAL CORD INJURY INDUCED INFLAMMATION NER01NS037130 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BETHEA, JOHN ROLAND · 1999 to 2002
$663k
NINDS NIH HHS NS37130NINDS NIH HHS R01 NS037130
6 · The paper itself

Abstract

The transcription factor NF-kappaB plays an important role in both physiological and pathological events in the central nervous system. Nevertheless, the mechanisms of NF-kappaB-mediated regulation of gene expression, and the signaling molecules participating in the NF-kappaB pathway in the central nervous system are, to date, poorly understood. To identify such molecules, we conducted a yeast two-hybrid screen of a human brain cDNA library using NIK as bait. As a result, we identified a novel NIK and IKK(beta) binding protein designated NIBP that is mainly expressed in brain, muscle, heart, and kidney. Interestingly, low levels of expression were detected in immune tissues such as spleen, thymus, and peripheral blood leukocytes, where NF-kappaB is known to modulate immune function. We demonstrated by immunohistochemistry that NIBP expression in the brain is localized to neurons. NIBP physically interacts with NIK, IKK(beta), but not IKK(alpha) or IKK(gamma). NIBP overexpression potentiates tumor necrosis factor-alpha-induced NF-kappaB activation through increased phosphorylation of the IKK complex and its downstream I(kappa)B(alpha) and p65 substrates. Finally, knockdown of NIBP expression by small interfering RNA reduces tumor necrosis factor-alpha-induced NF-kappaB activation, prevents nerve growth factor-induced neuronal differentiation, and decreases Bcl-xL gene expression in PC12 cells. Our data demonstrate that NIBP, by interacting with NIK and IKK(beta), is a new enhancer of the cytokine-induced NF-(kappa)B signaling pathway. Because of its neuronal expression, we propose that NIBP may be a potential target for modulating the NF-(kappa)B signaling cascade in neuronal pathologies dependent upon abnormal activation of this pathway.

Indexed as

AnimalsBase Sequencebcl-X ProteinBlotting, NorthernBlotting, WesternBrainCarrier ProteinsCell DifferentiationCloning, MolecularCytokinesDNA, ComplementaryEnzyme ActivationGene Expression Regulation, NeoplasticGenes, ReporterGenetic VectorsGlutathione TransferaseBCL2L1 protein, humanBcl2l1 protein, ratbcl-X ProteinCarrier ProteinsCHUK protein, humanCytokinesDNA, ComplementaryGlutathione TransferaseI-kappa B KinaseIKBKB protein, humanIKBKE protein, humanIntercellular Signaling Peptides and ProteinsNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2RNA, Small InterferingTRAPPC9 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID15951441
PMCPMC3707486
OpenAlexW2159114004

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.