Evidence map›Paper›PMID 24277482›Full record

ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2014

TNF-α/NF-κB signaling in the CNS: possible connection to EPHB2.

Paul D Pozniak, Martyn K White, Kamel Khalili

Abstract readReview
In one paragraph

Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 24% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  19. Exogenous 3-Iodothyronamine (TLife (Basel, Switzerland) · 2022
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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

3 authors at 2 institutions in 1 country.

Paul D PozniakCenter for Neurovirology, Department of Neuroscience, Temple University School of Medicine, Room 741 MERB, 3500N. Broad Street, Philadelphia, PA, 19140, USA.
Martyn K White
Kamel Khalili
Temple College · USTemple University · US

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Ilker Kudret Sariyer · 2011 to 2026
$24.9M
Interdisciplinary And Translational Research Training In NeurohivT32MH079785 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Kamel Khalili · 2008 to 2026
$5.4M
Cytokine regulation of JC virus latency and reactivationR01AI077460 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI WHITE, MARTYN K · 2008 to 2016
$3.2M
NIAID NIH HHS R01 AI077460NIMH NIH HHS P30 MH092177NIMH NIH HHS T32 MH079785
6 · The paper itself

Abstract

Tumor necrosis factor-alpha, TNF-α, is a cytokine that is a well-known factor in multiple disease conditions and is recognized for its major role in central nervous system signaling. TNF-α signaling is most commonly associated with neurotoxicity, but in some conditions it has been found to be neuroprotective. TNF-α has long been known to induce nuclear factor-kappa B, NF-κB, signaling by, in most cases, translocating the p65 (RelA) DNA binding factor to the nucleus. p65 is a key member of NF-κB, which is well established as a family of transcription factors that regulates many signaling events, including growth and process development, in neuronal cell populations. NF-κB has been shown to affect both the receiving aspect of neuronal signaling events in dendritic development as well as the sending of neuronal signals in axonal development. In both cases, NK-κB functions as a promoter and/or inhibitor of growth, depending on the environmental conditions and signaling cascade. In addition, NF-κB is involved in memory formation or neurogenesis, depending on the region of the brain in which the signaling occurs. The ephrin (Eph) receptor family represents a subfamily of receptor tyrosine kinases, RTKs, which received much attention due to its potential involvement in neuronal cell health and function. There are two subsets of ephrin receptors, Eph A and Eph B, each with distinct functions in cardiovascular and skeletal development and axon guidance and synaptic plasticity. The presence of multiple binding sites for NF-κB within the regulatory region of EphB2 gene and its potential regulation by NF-κB pathway suggests that TNF-α may modulate EphB2 via NF-κB and that this may contribute to the neuroprotective activity of TNF-α.

Indexed as

AnimalsCentral Nervous SystemHumansNF-kappa BReceptor, EphB2Signal TransductionTumor Necrosis Factor-alphaNF-kappa BReceptor, EphB2Tumor Necrosis Factor-alpha

Identifiers

PMID24277482
PMCPMC3959244
OpenAlexW2028644104

What OpenQuestion holds

Textmetadata
LicenceTDM
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.