Evidence map›Paper›PMID 30389842›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

An Alternative Exon of CAPS2 Influences Catecholamine Loading into LDCVs of Chromaffin Cells.

Olga Ratai, Claudia Schirra, Elvin Rajabov, Irene Brunk, Gudrun Ahnert-Hilger, Praneeth Chitirala, Ute Becherer, David R Stevens, Jens Rettig

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

9 authors at 2 institutions in 1 country.

Olga RataiDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and.
Claudia SchirraDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and.
Elvin RajabovDepartment of Integrative Anatomy, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany.
Irene BrunkDepartment of Integrative Anatomy, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany.
Gudrun Ahnert-HilgerDepartment of Integrative Anatomy, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany.
Praneeth ChitiralaDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and.
Ute BechererDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and.
David R StevensDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and.
Jens RettigDepartment of Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, 66421 Homburg, Germany, and jrettig@uks.eu.ORCID 0000-0001-6160-3954
Saarland University · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The calcium-dependent activator proteins for secretion (CAPS) are priming factors for synaptic and large dense-core vesicles (LDCVs), promoting their entry into and stabilizing the release-ready state. A modulatory role of CAPS in catecholamine loading of vesicles has been suggested. Although an influence of CAPS on monoamine transporter function and on vesicle acidification has been reported, a role of CAPS in vesicle loading is disputed. Using expression of naturally occurring splice variants of CAPS2 into chromaffin cells from CAPS1/CAPS2 double-deficient mice of both sexes, we show that an alternative exon of 40 aa is responsible for enhanced catecholamine loading of LDCVs in mouse chromaffin cells. The presence of this exon leads to increased activity of both vesicular monoamine transporters. Deletion of CAPS does not alter acidification of vesicles. Our results establish a splice-variant-dependent modulatory effect of CAPS on catecholamine content in LDCVs.

Indexed as

AnimalsCalcium-Binding ProteinsCatecholaminesCHO CellsChromaffin CellsCricetinaeCricetulusCytoplasmic VesiclesExonsFemaleHydrogen-Ion ConcentrationMaleMiceMice, KnockoutNerve Tissue ProteinsProtein IsoformsCalcium-Binding ProteinsCAPS2 protein, mouseCatecholaminesNerve Tissue ProteinsProtein IsoformsSerotoninVesicular Monoamine Transport Proteinsamperometrychromaffin cellsexocytosislarge dense-core vesiclesprimingreadily releasable pool

Identifiers

PMID30389842
PMCPMC6331651
OpenAlexW2899070891

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.