Evidence map›Paper›PMID 23028454›Full record

ArticlePloS one2012

Gene network revealed involvements of Birc2, Birc3 and Tnfrsf1a in anti-apoptosis of injured peripheral nerves.

Yongjun Wang, Xin Tang, Bin Yu, Yun Gu, Ying Yuan, Dengbing Yao, Fei Ding, Xiaosong Gu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. 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
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  4. Targeting the Hippo pathway in Schwann cells ameliorates peripheral nerve degeneration via a polypharmacological mechanism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
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  15. Streptococcal infection and immune response in children with Tourette's syndrome.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2015
    Observational
  16. Article
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  19. Altered expression of apoptotic genes in response to OCT4B1 suppression in human tumor cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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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

8 authors at 1 institution in 1 country.

Yongjun WangKey Laboratory of Neuroregeneration, Nantong University, Nantong, PR China.
Xin Tang
Bin Yu
Yun Gu
Ying Yuan
Dengbing Yao
Fei Ding
Xiaosong Gu
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crush injury or axotomy of peripheral nerves results in the rapid production of the inflammatory cytokines, which were confirmed in various models, to some extent, to be noxious to the myelin sheath or Schwann cells (SCs). TNF-α is one of the primary initiators of the inflammatory cascade and exerts pleiotropic functions in the physiological conditions by binding to its receptors, type I (TNFRI) and type II (TNFRII). The pathway molecules TNFRI, Birc2 and Birc3 play key roles during the activation of the signaling. Injured peripheral nerves, preventing them from TNF-α-mediated destruction and proceeding to successful regeneration, might initiate an anti-apoptotic mechanism. To identity the exact functions of TNFRI, Birc2 and Birc3, as well as its involved pathways in the cellular events, we inferred a dynamic gene regulatory network from short time-series measurements of the proximal nerve segment cDNA microarray following rat sciatic nerve transection. TNFRI family member Tnfrsf1a, Birc2 and Birc3 were mined out integrating as master regulators to mediate inflammatory responses. Experiments revealed that Tnfrsf1a, Birc2 and Birc3 proteins colocalized with S100 in the rat peripheral nerve tissues, and the expression levels increased with the time extension. Knockdown of the proteins induced the apoptotic formation of primary cultured SCs by upregulation of caspase 3 and caspase 6. Our systematic analysis indicated that Tnfrsf1a, Birc2 and Birc3 of SCs, not originally regarded as XIAP, were mainly responsible for the inflammation-mediated anti-apoptosis of peripheral nerves. Birc2 and Birc3 might be the most potential targets for anti-apoptotic protection mediated by inflammatory cytokines.

Indexed as

Gene Regulatory NetworksAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinCaspase 3Caspase 6Gene Expression ProfilingGene Expression RegulationInhibitor of Apoptosis ProteinsMalePeripheral Nerve InjuriesRatsRats, Sprague-DawleyReceptors, Tumor Necrosis Factor, Type IRNA InterferenceSchwann CellsBaculoviral IAP Repeat-Containing 3 ProteinBirc3 protein, ratCaspase 3Caspase 6Inhibitor of Apoptosis ProteinsReceptors, Tumor Necrosis Factor, Type ITumor Necrosis Factor-alpha

Identifiers

PMID23028454
PMCPMC3444457
OpenAlexW2092299008

What OpenQuestion holds

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LicenceCC BY
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.