Evidence map›Paper›PMID 25664921›Full record

ArticleChannels (Austin, Tex.)2015

A new genetic model for calcium induced autophagy and ER-stress in Drosophila photoreceptor cells.

Shirley Weiss, Baruch Minke

Open access · goldAbstract read
In one paragraph

Article in Channels (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 10 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

2 authors at 2 institutions in 2 countries.

Shirley Weissa Department of Medical Neurobiology ; Institute for Medical Research Israel-Canada (IMRIC) and the Edmond and Lily Safra Center for Brain Sciences (ELSC); Faculty of Medicine; The Hebrew University ; Jerusalem , Israel.
Baruch Minke
Faculty (United Kingdom) · GBHebrew College · US

Funding

GENETIC DISSECTION OF PHOTOTRANSDUCTIONR01EY003529 · NEI · HEBREW UNIVERSITY OF JERUSALEM · PI MINKE, BARUCH · 1985 to 2011
$1.8M
NEI NIH HHS R01 EY 03529
6 · The paper itself

Abstract

Cytoplasmic Ca2+ overload is known to trigger autophagy and ER-stress. Furthermore, ER-stress and autophagy are commonly associated with degenerative pathologies, but their role in disease progression is still a matter of debate, in part, owing to limitations of existing animal model systems. The Drosophila eye is a widely used model system for studying neurodegenerative pathologies. Recently, we characterized the Drosophila protein, Calphotin, as a cytosolic immobile Ca2+ buffer, which participates in Ca2+ homeostasis in Drosophila photoreceptor cells. Exposure of calphotin hypomorph flies to continuous illumination, which induces Ca2+ influx into photoreceptor cells, resulted in severe Ca2+-dependent degeneration. Here we show that this degeneration is autophagy and ER-stress related. Our studies thus provide a new model in which genetic manipulations trigger changes in cellular Ca2+ distribution. This model constitutes a framework for further investigations into the link between cytosolic Ca2+, ER-stress and autophagy in human disorders and diseases.

Indexed as

Models, GeneticAnimalsAutophagyCalciumDisease Models, AnimalDrosophilaEndoplasmic Reticulum StressPhotoreceptor Cells, InvertebrateCalciumautophagycalcium homeostasiscalphotincalphotin- Cpncalphotin hypomorph- Cpn1%dMoesin- MoeDrosophilaER-stressphotoreceptor cellsTransient receptor potential- TRP

Identifiers

PMID25664921
PMCPMC4594479
OpenAlexW2092368687

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.