Evidence map›Paper›PMID 21738764›Full record

ArticlePloS one2011

Mitochondrial localized STAT3 is involved in NGF induced neurite outgrowth.

Lihan Zhou, Heng-Phon Too

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  14. IL-6 enhances CD4 cell motility by sustaining mitochondrial CaProceedings of the National Academy of Sciences of the United States of America · 2021
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  17. An Update on the Multifaceted Roles of STAT3 in the Heart.Frontiers in cardiovascular medicine · 2019
    Review
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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

2 authors at 2 institutions in 2 countries.

Lihan ZhouDepartment of Biochemistry, National University of Singapore, Singapore, Singapore.
Heng-Phon Too
Massachusetts Institute of Technology · USSingapore-MIT Alliance for Research and Technology · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignal transducer and activator of transcription 3 (STAT3) plays critical roles in neural development and is increasingly recognized as a major mediator of injury response in the nervous system. Cytokines and growth factors are known to phosphorylate STAT3 at tyrosine(705) with or without the concomitant phosphorylation at serine(727), resulting in the nuclear localization of STAT3 and subsequent transcriptional activation of genes. Recent evidence suggests that STAT3 may control cell function via alternative mechanisms independent of its transcriptional activity. Currently, the involvement of STAT3 mono-phosphorylated at residue serine(727) (P-Ser-STAT3) in neurite outgrowth and the underlying mechanism is largely unknown. PRINCIPAL

findingsIn this study, we investigated the role of nerve growth factor (NGF) induced P-Ser-STAT3 in mediating neurite outgrowth. NGF induced the phosphorylation of residue serine(727) but not tyrosine(705) of STAT3 in PC12 and primary cortical neuronal cells. In PC12 cells, serine but not tyrosine dominant negative mutant of STAT3 was found to impair NGF induced neurite outgrowth. Unexpectedly, NGF induced P-Ser-STAT3 was localized to the mitochondria but not in the nucleus. Mitochondrial STAT3 was further found to be intimately involved in NGF induced neurite outgrowth and the production of reactive oxygen species (ROS).

conclusionTaken together, the findings herein demonstrated a hitherto unrecognized novel transcription independent mechanism whereby the mitochondria localized P-Ser-STAT3 is involved in NGF induced neurite outgrowth.

Indexed as

AnimalsMitochondriaNerve Growth FactorNeuritesPC12 CellsRatsSTAT3 Transcription FactorNerve Growth FactorSTAT3 Transcription Factor

Identifiers

PMID21738764
PMCPMC3124549
OpenAlexW2043082088

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Registered trials

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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.