Evidence map›Paper›PMID 27412116›Full record

ArticleNeurochemical research2017

Ammonium Increases TRPC1 Expression Via Cav-1/PTEN/AKT/GSK3β Pathway.

Wei Wang, Li Gu, Alexei Verkhratsky, Liang Peng

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. 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

4 authors at 2 institutions in 3 countries.

Wei WangLaboratory of Metabolic Brain Diseases, Institute of Metabolic Disease Research and Drug Development, China Medical University, No. 77, Puhe Road, Shenbei District, Shenyang, People's Republic of China.
Li GuLaboratory of Metabolic Brain Diseases, Institute of Metabolic Disease Research and Drug Development, China Medical University, No. 77, Puhe Road, Shenbei District, Shenyang, People's Republic of China.
Alexei VerkhratskyFaculty of Life Science, The University of Manchester, Manchester, UK.
Liang PengLaboratory of Metabolic Brain Diseases, Institute of Metabolic Disease Research and Drug Development, China Medical University, No. 77, Puhe Road, Shenbei District, Shenyang, People's Republic of China. hkkid08@yahoo.com.
China Medical University · CNUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperammonemia occurring following acute liver failure is the primary cause of hepatic encephalopathy. In the brain, ammonium is catabolised by glutamine synthetase expressed exclusively in astroglia; ammonium overload impairs astroglial homeostatic systems. Previously, we had reported that chronic treatment with 3 mM ammonia increased expression of transient receptor potential canonic 1 (TRPC1) channels and Ca

Indexed as

AmmoniaAnimalsAstrocytesCaveolin 1Cell MembraneCells, CulturedFemaleGlycogen Synthase Kinase 3 betaHyperammonemiaMaleMiceMice, TransgenicPhosphorylationProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, Small InterferingAmmoniaCav1 protein, mouseCaveolin 1Glycogen Synthase Kinase 3 betaProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseRNA, Small Interferingtransient receptor potential cation channel, subfamily C, member 1TRPC Cation ChannelsAmmoniumAstrocyteCav-1, PTEN, PI3K/AKTGSK-3βHepatic encephalopathy

Identifiers

PMID27412116
OpenAlexW2465220456

What OpenQuestion holds

Textmetadata
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.