Evidence map›Paper›PMID 15930141›Full record

ArticleAmerican journal of physiology. Cell physiology2005

Dominant-negative PKC-epsilon impairs apical actin remodeling in parallel with inhibition of carbachol-stimulated secretion in rabbit lacrimal acini.

Galina V Jerdeva, Francie A Yarber, Melvin D Trousdale, Christopher J Rhodes, Curtis T Okamoto, Darlene A Dartt, Sarah F Hamm-Alvarez

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. INTRACELLULAR SIGNALING BY BILE ACIDS.Journal of bio-science · 2012
    Article
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  12. 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

7 authors at 3 institutions in 2 countries.

Galina V JerdevaDepartment of Pharmaceutical Sciences, University of Southern California School of Pharmacy, 1985 Zonal Ave., Los Angeles, California 90033, USA.
Francie A Yarber
Melvin D Trousdale
Christopher J Rhodes
Curtis T Okamoto
Darlene A Dartt
Sarah F Hamm-Alvarez
Pacific Northwest Diabetes Research Institute · USPharmaceutical Biotechnology (Czechia) · CZLAC+USC Medical Center · US

Funding

Research Supplements to Promote DiversityR01EY011386 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAMM-ALVAREZ, SARAH F · 1996 to 2025
$9.3M
MECHANISM OF LACRIMAL GLAND SECRETIONR01EY006177 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI DARTT, DARLENE A · 1985 to 2012
$5.7M
PEPT1: STRUCTURE-FUNCTION, SORTING AND MODULATIONR01GM059297 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAWORTH, IAN S · 2000 to 2003
$1.3M
VESICLE TRANSPORT REGULATION IN INTOXICATION AND DISEASER01DK056040 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RUNNEGAR, MARIA T · 1999 to 2003
$1.1M
MECHANISMS OF HSV-1 TRANSPORT IN CNS NEURONSR01NS038246 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GARNER, JUDY ANN · 2000 to 2003
$1.0M
Adenovirus Modulation of Lacrimal Gland FunctionR03EY013949 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAMM-ALVAREZ, SARAH F · 2003 to 2005
$488k
NEI NIH HHS EY-05081NEI NIH HHS EY-06177NEI NIH HHS EY-11386NEI NIH HHS EY-13949NEI NIH HHS R01 EY006177NEI NIH HHS R01 EY011386NEI NIH HHS R03 EY013949NIDDK NIH HHS DK-56040NIDDK NIH HHS R01 DK056040NIGMS NIH HHS GM-59297NIGMS NIH HHS R01 GM059297NINDS NIH HHS NS-38246NINDS NIH HHS R01 NS038246
6 · The paper itself

Abstract

We investigated the involvement of PKC-epsilon in apical actin remodeling in carbachol-stimulated exocytosis in reconstituted rabbit lacrimal acinar cells. Lacrimal acinar PKC-epsilon cosedimented with actin filaments in an actin filament binding assay. Stimulation of acini with carbachol (100 microM, 2-15 min) significantly (P < or = 0.05) increased PKC-epsilon recovery with actin filaments in two distinct biochemical assays, and confocal fluorescence microscopy showed a significant increase in PKC-epsilon association with apical actin in stimulated acini as evidenced by quantitative colocalization analysis. Overexpression of dominant-negative (DN) PKC-epsilon in lacrimal acini with replication-defective adenovirus (Ad) resulted in profound alterations in apical and basolateral actin filaments while significantly inhibiting carbachol-stimulated secretion of bulk protein and beta-hexosaminidase. The chemical inhibitor GF-109203X (10 microM, 3 h), which inhibits PKC-alpha, -beta, -delta, and -epsilon, also elicited more potent inhibition of carbachol-stimulated secretion relative to Gö-6976 (10 microM, 3 h), which inhibits only PKC-alpha and -beta. Transduction of lacrimal acini with Ad encoding syncollin-green fluorescent protein (GFP) resulted in labeling of secretory vesicles that were discharged in response to carbachol stimulation, whereas cotransduction of acini with Ad-DN-PKC-epsilon significantly inhibited carbachol-stimulated release of syncollin-GFP. Carbachol also increased the recovery of secretory component in culture medium, whereas Ad-DN-PKC-epsilon transduction suppressed its carbachol-stimulated release. We propose that DN-PKC-epsilon alters lacrimal acinar apical actin remodeling, leading to inhibition of stimulated exocytosis and transcytosis.

Indexed as

ActinsAnimalsCarbacholCarrier ProteinsExocytosisFemaleIsoenzymesLacrimal ApparatusMembrane ProteinsProtein Kinase CProtein Kinase C-epsilonRabbitsActinsCarbacholCarrier ProteinsIsoenzymesMembrane ProteinsProtein Kinase CProtein Kinase C-epsilonSycn protein, rat

Identifiers

PMID15930141
PMCPMC1414898
OpenAlexW2138947981

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.