Evidence map›Paper›PMID 19166928›Full record

ArticleCellular signalling2009

Gastrointestinal growth factors and hormones have divergent effects on Akt activation.

Marc J Berna, Jose A Tapia, Veronica Sancho, Michelle Thill, Andrea Pace, K Martin Hoffmann, Lauro Gonzalez-Fernandez, Robert T Jensen

Open access · greenAbstract readComparative Study
In one paragraph

Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 32 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 4 countries.

Marc J BernaDigestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-1804, USA.
Jose A Tapia
Veronica Sancho
Michelle Thill
Andrea Pace
K Martin Hoffmann
Lauro Gonzalez-Fernandez
Robert T Jensen
National Institute of Diabetes and Digestive and Kidney Diseases · USUniversidad de Extremadura · ESUniversity Medical Center Hamburg-Eppendorf · DEMedical University of Graz · ATNational Eye Institute · US

Funding

Cellular Basis Of Action Of Gastrointestinal Peptides/Growth factorsZIADK053101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 2009 to 2025
$12.9M
Characterization And Pharmacology Of Receptors For Gastrointestinal PeptidesZIADK053100 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 2009 to 2025
$12.7M
Cellular Basis Of Action Of Gastrointestinal Peptides/Growth factorsZ01DK053101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 1990 to 2008
$726k
IDENTIFICATION AND CHARACTERIZATION OF RECEPTORS FOR GI PEPTIDESZ01DK053100 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 1990 to 2008
$724k
Intramural NIH HHS Z01 DK053100Intramural NIH HHS Z01 DK053101
6 · The paper itself

Abstract

Akt is a central regulator of apoptosis, cell growth and survival. Growth factors and some G-protein-coupled receptors (GPCR) regulate Akt. Whereas growth-factor activation of Akt has been extensively studied, the regulation of Akt by GPCR's, especially gastrointestinal hormones/neurotransmitters, remains unclear. To address this area, in this study the effects of GI growth factors and hormones/neurotransmitters were investigated in rat pancreatic acinar cells which are high responsive to these agents. Pancreatic acini expressed Akt and 5 of 7 known pancreatic growth-factors stimulate Akt phosphorylation (T308, S473) and translocation. These effects are mediated by p85 phosphorylation and activation of PI3K. GI hormones increasing intracellular cAMP had similar effects. However, GI-hormones/neurotransmitters [CCK, bombesin, carbachol] activating phospholipase C (PLC) inhibited basal and growth-factor-stimulated Akt activation. Detailed studies with CCK, which has both physiological and pathophysiological effects on pancreatic acinar cells at different concentrations, demonstrated CCK has a biphasic effect: at low concentrations (pM) stimulating Akt by a Src-dependent mechanism and at higher concentrations (nM) inhibited basal and stimulated Akt translocation, phosphorylation and activation, by de-phosphorylating p85 resulting in decreasing PI3K activity. This effect required activation of both limbs of the PLC-pathway and a protein tyrosine phosphatase, but was not mediated by p44/42 MAPK, Src or activation of a serine phosphatase. Akt inhibition by CCK was also found in vivo and in Panc-1 cancer cells where it inhibited serum-mediated rescue from apoptosis. These results demonstrate that GI growth factors as well as gastrointestinal hormones/neurotransmitters with different cellular basis of action can all regulate Akt phosphorylation in pancreatic acinar cells. This regulation is complex with phospholipase C agents such as CCK, because both stimulatory and inhibitory effects can be seen, which are mediated by different mechanisms.

Indexed as

AnimalsCalciumCell Line, TumorCyclic AMPEnzyme ActivationEnzyme InhibitorsGastrointestinal HormonesIntercellular Signaling Peptides and ProteinsMaleNeurotransmitter AgentsPancreasPancreatic NeoplasmsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Kinase CAkt1 protein, ratCalciumCyclic AMPEnzyme InhibitorsGastrointestinal HormonesIntercellular Signaling Peptides and ProteinsNeurotransmitter AgentsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase CProto-Oncogene Proteins c-aktReceptor, Cholecystokinin ASincalidesrc-Family KinasesType C Phospholipases

Identifiers

PMID19166928
PMCPMC2677382
OpenAlexW2065632763

What OpenQuestion holds

Textmetadata
LicenceTDM
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.