Evidence map›Paper›PMID 26721511›Full record

ArticleNeurochemical research2016

Noncanonical Activin A Signaling in PC12 Cells: A Self-Limiting Feedback Loop.

Jiao-Qi Wang, Wen-Zhao Liang, Yang Cui, Jin-Ting He, Hong-Yu Liu, Yue Wang, Long-Xing Xue, Qiu-Ye Ji, Wei Shi, Yan-Kun Shao and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

12 authors.

Jiao-Qi WangDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Wen-Zhao LiangDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Yang CuiDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Jin-Ting HeDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Hong-Yu LiuDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Yue WangDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Long-Xing XueDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Qiu-Ye JiResearch Center, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Wei ShiKey Laboratory for Molecular Enzymology and Engineering, The Ministry of Education, Jilin University, 2699 Qianjin Street, Changchun, 130012, China.
Yan-Kun ShaoDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China.
Jing MangDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China. mangjing@jlu.edu.cn.
Zhong-Xin XuDepartment of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun, 130012, China. xuzhongxin999@aliyun.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activin A (Act A), a member of transforming growth factor-β superfamily, plays a neuroprotective role in multiple neurological diseases through Act A/Smads signal activation. Traditionally, the up-regulation of Act A gene and extracellular Act A accumulation show the signal activation as a linear pathway. However, one of our discoveries indicated that Act A could lead a loop signaling in ischemic injury. To clarify the characteristic of this loop signaling in a non-pathological state, we up-regulated the expression of Act A, monitored extracellular Act A accumulation and examined the activity of Act A signaling, which was quantified by the expression of phosphorylated Smad3 and the fluorescence intensity of Smad4 in nuclei. The results demonstrated a noncanonical Act A signal loop with self-amplifying property in PC12 cells. Further, it showed self-limiting behavior due to temporary activation and spontaneous attenuation. This periodic behavior of Act A signal loop was found to be regulated by the level of Smad anchor for receptor activation (SARA). Moreover, increased activity of Act A signal loop could promote PC12 cell proliferation and enhance the survival rate of cells to Oxygen-Glucose Deprivation. These practical discoveries will bring new insight on the functional outcome of Act A signaling in neurological diseases by the further understanding: loop signaling.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell ProliferationCell SurvivalFeedbackGlucoseInhibin-beta SubunitsOxygenPC12 CellsPhosphorylationRatsRecombinant ProteinsSignal TransductionSmad3 ProteinSmad4 ProteinAdaptor Proteins, Signal TransducingGlucoseinhibin beta A subunitInhibin-beta SubunitsOxygenRecombinant ProteinsSmad3 ProteinSmad3 protein, ratSmad4 ProteinSmad4 protein, ratZfyve9 protein, ratActivin ASignaling loopSmad anchor for receptor activation

Identifiers

PMID26721511

What OpenQuestion holds

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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.