Evidence map›Paper›PMID 15044551›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Insulinoma-Associated Protein IA-2, a Vesicle Transmembrane Protein, Genetically Interacts with UNC-31/CAPS and Affects Neurosecretion in Caenorhabditis elegans.

Tao Cai, Tetsunari Fukushige, Abner L Notkins, Michael Krause

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

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  8. Homeostatic Feedback Modulates the Development of Two-State Patterned Activity in a Model Serotonin Motor Circuit inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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  16. Advances in the cellular immunological pathogenesis of type 1 diabetes.Journal of cellular and molecular medicine · 2014
    Review
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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

4 authors at 2 institutions in 1 country.

Tao CaiExperimental Medicine Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
Tetsunari Fukushige
Abner L Notkins
Michael Krause
National Institute of Dental and Craniofacial Research · USNational Institutes of Health · US

Funding

Insulin-Dependent Diabetes MellitusZIADE000423 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI NOTKINS, ABNER L. · 2009 to 2020
$16.9M
INSULIN-DEPENDENT DIABETES MELLITUSZ01DE000423 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI NOTKINS, ABNER L. · 1986 to 2008
$3.5M
6 · The paper itself

Abstract

IA-2 (insulinoma-associated protein 2), a major autoantigen in type 1 diabetes, is a receptor-tyrosine phosphatase-like protein associated with the membrane of secretory granules of neural and endocrine-specific cells. Loss of IA-2 activity in the mouse results in reduced insulin release and additional phenotypes, consistent with a general effect on neurosecretion and hormone release. To gain further insight into the cellular mechanisms of IA-2 function, we have studied the Caenorhabditis elegans homolog, CeIA-2 encoded by the ida-1 gene. Using two independent putative null alleles of ida-1, we demonstrate that animals lacking CeIA-2 activity are viable and exhibit subtle defects. Genetic studies of mutants in ida-1 and several genes involved in neurosecretory vesicle cargo release and signaling highlight two roles for CeIA-2. First, CeIA-2 has a specific and novel genetic interaction with UNC-31/CAPS, a protein that has been shown in other systems to regulate dense-core vesicle cargo release. Second, loss of CeIA-2 activity enhances weak alleles in the insulin-like signaling pathway. These results suggest that CeIA-2 may be an important factor in dense-core vesicle cargo release with parallels to insulin signaling in mammals.

Indexed as

AldicarbAllelesAnimalsAutoantigensCaenorhabditis elegansCaenorhabditis elegans ProteinsCalcium-Binding ProteinsDrug ResistanceGene Expression RegulationGreen Fluorescent ProteinsLuminescent ProteinsMembrane GlycoproteinsMembrane ProteinsMotor ActivityNerve Tissue ProteinsNeurosecretionAldicarbAutoantigensCaenorhabditis elegans ProteinsCalcium-Binding ProteinsGreen Fluorescent ProteinsIDA-1 protein, C elegansLuminescent ProteinsMembrane GlycoproteinsMembrane ProteinsNerve Tissue ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine PhosphatasesPtprn protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 8Recombinant Fusion ProteinsSynaptotagminsUNC-31 protein, C elegans

Identifiers

PMID15044551
PMCPMC6729843
OpenAlexW2115622859

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.