Evidence map›Paper›PMID 26238084›Full record

ArticleMolecular and cellular endocrinology2015

Role of PI4K and PI3K-AKT in ERK1/2 activation by GnRH in the pituitary gonadotropes.

Tali H Bar-Lev, Dagan Harris, Melanija Tomić, Stanko Stojilkovic, Zeev Blumenfeld, Pamela Brown, Rony Seger, Zvi Naor

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

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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

8 authors at 5 institutions in 3 countries.

Tali H Bar-LevDepartment of Biochemistry and Molecular Biology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Ramat Aviv 69978, Israel.
Dagan HarrisDepartment of Biochemistry and Molecular Biology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Ramat Aviv 69978, Israel.
Melanija TomićNational Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD 20892-4510, USA.
Stanko StojilkovicNational Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD 20892-4510, USA.
Zeev BlumenfeldReproductive Endocrinology, OB/GYN, Rambam Health Care Campus, Technion-Faculty of Medicine, Haifa 31096, Israel.
Pamela BrownMedical Research Council (MRC) Centre of Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, Scotland EH16 4TJ, United Kingdom.
Rony SegerDepartment of Biological Regulation, the Weizmann Institute of Science, Rehovot 76100, Israel.
Zvi NaorDepartment of Biochemistry and Molecular Biology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Ramat Aviv 69978, Israel. Electronic address: ZviN@tauex.tau.ac.il.
Tel Aviv University · ILEunice Kennedy Shriver National Institute of Child Health and Human Development · USMRC Centre for Reproductive Health · GBRambam Health Care Campus · ILWeizmann Institute of Science · IL

Funding

Intracellular Signaling In Endocrine CellsZIAHD000195 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STOJILKOVIC, STANKO S. · 2009 to 2025
$18.8M
Intramural NIH HHS ZIA HD000195
6 · The paper itself

Abstract

The role of PI4K and PI3K-AKT in ERK1/2 activation by GnRH was examined. A relatively long preincubation (60 min) with wortmannin (10 nM and 10 μM), and LY294002 (10 μM and 100 μM) (doses known to inhibit PI3K and PI4K, respectively), were required to inhibit GnRH-and PMA-stimulated ERK1/2 activity in αT3-1 and LβT2 gonadotrope cells. A similar preincubation protocol was required to demonstrate inhibition of IGF-1-stimulated AKT activation lending support for the need of prolonged incubation (60 min) with wortmannin in contrast to other cellular systems. To rule out that the inhibitors acted upon PI(4,5)P2 levels, we followed the [Ca(2+)]i response to GnRH and found that wortmannin has no significant effect on GnRH-induced [Ca(2+)]i responses. Surprisingly, GnRH and PMA reduced, while IGF-1 increased AKT phosphorylation. We suggest that PI3K inhibits GnRH-stimulated αGSU activity, has no effect upon GnRH-stimulated LHβ activity and enhanced the GnRH-stimulated FSHβ transcription. Hence, PI4K and PI3K-AKT play a role in GnRH to ERK1/2 signaling, while PI3K may regulate also GnRH-induced gonadotropin gene expression.

Indexed as

1-Phosphatidylinositol 4-KinaseAndrostadienesAnimalsCell LineChromonesGonadotrophsGonadotropin-Releasing HormoneGonadotropinsMAP Kinase Signaling SystemMiceMorpholinesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktWortmannin1-Phosphatidylinositol 4-Kinase2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAndrostadienesChromonesGonadotropin-Releasing HormoneGonadotropinsMorpholinesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktWortmanninERK1/2GnRHGonadotropesLβT2 cellsMAPKPI3KPI4KPKCαT3-1 cells

Identifiers

PMID26238084
PMCPMC4582010
OpenAlexW970847131

What OpenQuestion holds

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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.