Evidence map›Paper›PMID 16407557›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Single transmembrane domain insulin-like growth factor-II/mannose-6-phosphate receptor regulates central cholinergic function by activating a G-protein-sensitive, protein kinase C-dependent pathway.

Cheryl Hawkes, Jack H Jhamandas, Kim H Harris, Wen Fu, Richard G MacDonald, Satyabrata Kar

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 86 citations in OpenAlex.

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  16. Insulin-Like Growth Factor II Targets the mTOR Pathway to Reverse Autism-Like Phenotypes in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

6 authors at 3 institutions in 2 countries.

Cheryl HawkesDepartment of Neurology and Neurosurgery, McGill University, Montreal, Quebec, H3A 2B4, Canada.
Jack H Jhamandas
Kim H Harris
Wen Fu
Richard G MacDonald
Satyabrata Kar
University of Alberta · CAMcGill University · CAUniversity of Nebraska Medical Center · US

Funding

Molecular Dissection of IGF2R Growth Suppressor ActivityR01CA091885 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MACDONALD, RICHARD G. · 2001 to 2004
$659k
NCI NIH HHS CA91885NCI NIH HHS R01 CA091885
6 · The paper itself

Abstract

The insulin-like growth factor-II/mannose-6-phosphate (IGF-II/M6P) receptor is a single-pass transmembrane glycoprotein that plays an important role in the intracellular trafficking of lysosomal enzymes and endocytosis-mediated degradation of IGF-II. However, its role in signal transduction after IGF-II binding remains unclear. In the present study, we report that IGF-II/M6P receptor in the rat brain is coupled to a G-protein and that its activation by Leu27IGF-II, an analog that binds rather selectively to the IGF-II/M6P receptor, potentiates endogenous acetylcholine release from the rat hippocampal formation. This effect is mediated by a pertussis toxin (PTX)-sensitive GTP-binding protein and is dependent on protein kinase Calpha (PKCalpha)-induced phosphorylation of downstream substrates, myristoylated alanine-rich C kinase substrate, and growth associated protein-43. Additionally, treatment with Leu27IGF-II causes a reduction in whole-cell currents and depolarization of cholinergic basal forebrain neurons. This effect, which is blocked by an antibody against the IGF-II/M6P receptor, is also sensitive to PTX and is mediated via activation of a PKC-dependent pathway. These results together revealed for the first time that the single transmembrane domain IGF-II/M6P receptor expressed in the brain is G-protein coupled and is involved in the regulation of central cholinergic function via the activation of specific intracellular signaling cascades.

Indexed as

AcetylcholineAmino Acid SubstitutionAnimalsBinding, CompetitiveCholera ToxinDelayed Rectifier Potassium ChannelsGAP-43 ProteinGTP-Binding Protein alpha Subunit, Gi2Guanosine 5'-O-(3-Thiotriphosphate)Guanylyl ImidodiphosphateHippocampusInsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIIntracellular Signaling Peptides and ProteinsIsoproterenolAcetylcholineCholera ToxinDelayed Rectifier Potassium ChannelsGAP-43 ProteinGTP-Binding Protein alpha Subunit, Gi2Guanosine 5'-O-(3-Thiotriphosphate)Guanylyl ImidodiphosphateiberiotoxinInsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIinsulin-like growth factor II, Leu(27)-Intracellular Signaling Peptides and ProteinsIsoproterenolMembrane ProteinsMyristoylated Alanine-Rich C Kinase SubstrateNerve Tissue ProteinsPeptidesPertussis ToxinPotassium Channel BlockersPotassium Channels, Calcium-ActivatedProtein Kinase C-alphaReceptor, IGF Type 2Receptors, G-Protein-Coupled

Identifiers

PMID16407557
PMCPMC6674423
OpenAlexW2128084065

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.