Evidence map›Paper›PMID 16378242›Full record

ArticleCellular and molecular life sciences : CMLS2006

Multiple cAMP-induced signaling cascades regulate prolactin expression in T cells.

S Gerlo, P Verdood, E L Hooghe-Peters, R Kooijman

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Cell physiology of cAMP sensor Epac.The Journal of physiology · 2006
    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

4 authors at 1 institution in 1 country.

S GerloNeuroendocrine Immunology Research Group, Department of Pharmacology, Free University of Brussels (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium.
P Verdood
E L Hooghe-Peters
R Kooijman
UCLouvain Saint-Louis Brussels · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beside its pivotal role in reproduction, the pituitary hormone prolactin (PRL) has been attributed an immunomodulatory function. Here we report that cAMP is an important stimulator of PRL transcription in primary human T lymphocytes. Inhibition of both protein kinase A (PKA) and p38 MAPK partially abrogated cAMP-induced PRL expression. In addition, cAMP-induced phosphorylation of p38 was shown to occur independently of PKA and could be mimicked by a methylated cAMP analogue which specifically activates the recently discovered cAMP receptor EPAC (exchange protein directly activated by cAMP). Our findings suggest that cAMP induces PRL expression in T lymphocytes via cooperation of at least two different signaling pathways: a PKA-dependent pathway leading to the phosphorylation of cAMP response element-binding protein, and a PKA-independent pathway leading to p38 phosphorylation.

Indexed as

Cells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesGene Expression RegulationGuanine Nucleotide Exchange FactorsHumansMitogen-Activated Protein KinasesProlactinRNA, MessengerSignal TransductionT-LymphocytesTranscription, GeneticCyclic AMPCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange FactorsMitogen-Activated Protein KinasesProlactinRAPGEF3 protein, humanRNA, Messenger

Identifiers

PMID16378242
PMCPMC2792358
OpenAlexW2065612361

What OpenQuestion holds

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LicenceCC BY-NC
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.