Evidence map›Paper›PMID 22710799›Full record

ArticleCell research2012

InsP3R-Ca(2+) signaling takes center stage in the hormonal regulation of hepatic gluconeogenesis.

Michihiro Matsumoto

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 94% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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

1 author at 1 institution in 1 country.

Michihiro MatsumotoDepartment of Molecular Metabolic Regulation, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan. mmatsumoto@ri.ncgm.go.jp
National Center for Global Health and Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During fasting, dephosphorylation-dependent activation of the CREB coactivator CRTC2 by glucagon is crucial for activation of the hepatic gluconeogenic program, but the molecular mechanism by which hormones regulate CRTC2 activation remains unclear. A recent report in Nature showed that PKA-dependent phosphorylation of the inositol-1,4,5-trisphosphate receptor (InsP3R) induces Ca mobilization, leading to increase in the phosphatase activity of calcineurin and the subsequent dephosphorylation of CRTC2, thereby resulting in the induction of gluconeogenic gene expression. It also showed that insulin-dependent phosphorylation of InsP3R by Akt inhibits Ca mobilization and CRTC2 dephosphorylation, resulting in the suppression of gluconeogenesis.

Indexed as

Calcium SignalingGluconeogenesisCalcineurinCalciumCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinHepatocytesInositol 1,4,5-Trisphosphate ReceptorsLiverPhosphorylationProto-Oncogene Proteins c-aktTranscription FactorsCalcineurinCalciumCRTC2 protein, humanCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinInositol 1,4,5-Trisphosphate ReceptorsProto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID22710799
PMCPMC3494392
OpenAlexW1983838791

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.