Evidence map›Paper›PMID 22105777›Full record

ArticleGlia2012

Emerging roles of p53 in glial cell function in health and disease.

Joseph D Jebelli, Claudie Hooper, Gwenn A Garden, Jennifer M Pocock

Abstract read
In one paragraph

Article in Glia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-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

19 citing papers in PubMed, 32 citations in OpenAlex.

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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

4 authors at 4 institutions in 3 countries.

Joseph D JebelliDepartment of Neuroinflammation, UCL Institute of Neurology, London, United Kingdom.
Claudie Hooper
Gwenn A Garden
Jennifer M Pocock
King's College London · GBUCL Australia · AUUniversity College London · GBUniversity of Washington · US

Funding

Molecular Regulation of Microglia BehaviorR01NS073848 · NINDS · UNIVERSITY OF WASHINGTON · PI GARDEN, GWENN A · 2011 to 2016
$1.7M
NINDS NIH HHS R01 NS073848
6 · The paper itself

Abstract

Emerging evidence suggests that p53, a tumor suppressor protein primarily involved in cancer biology, coordinates a wide range of novel functions in the CNS including the mediation of pathways underlying neurodegenerative disease pathogenesis. Moreover, an evolving concept in cell and molecular neuroscience is that glial cells are far more fundamental to disease progression than previously thought, which may occur via a noncell-autonomous mechanism that is heavily dependent on p53 activities. As a crucial hub connecting many intracellular control pathways, including cell-cycle control and apoptosis, p53 is ideally placed to coordinate the cellular response to a range of stresses. Although neurodegenerative diseases each display a distinct and diverse molecular pathology, apoptosis is a widespread hallmark feature and the multimodal capacity of the p53 system to orchestrate apoptosis and glial cell behavior highlights p53 as a potential unifying target for therapeutic intervention in neurodegeneration.

Indexed as

AnimalsHumansNervous System DiseasesNeurogliaNeuronsSignal TransductionTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID22105777
PMCPMC4195591
OpenAlexW2035531864

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.