(Q24304081)

positive regulation of calcium ion transport

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

author name string

Daisuke Takei

1

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Hisamitsu Ishihara

2

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Suguru Yamaguchi

3

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Takahiro Yamada

4

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Akira Tamura

5

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Hideki Katagiri

6

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Yoshio Maruyama

7

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Yoshitomo Oka

The versatility and universality of calcium signalling

8

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language of work or name

English

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publication date

16 October 2006

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published in

FEBS Letters

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volume

580

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issue

24

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page(s)

5635-40

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cites work

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2006.09.007

When calcium goes wrong: genetic alterations of a ubiquitous signaling route

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The endoplasmic reticulum Ca2+ store: a view from the lumen

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Store-operated calcium channels

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The mammalian unfolded protein response

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A gene encoding a transmembrane protein is mutated in patients with diabetes mellitus and optic atrophy (Wolfram syndrome)

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Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein

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WFS1 (Wolfram syndrome 1) gene product: predominant subcellular localization to endoplasmic reticulum in cultured cells and neuronal expression in rat brain

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Disruption of the WFS1 gene in mice causes progressive beta-cell loss and impaired stimulus-secretion coupling in insulin secretion

21 January 2018

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Mice conditionally lacking the Wolfram gene in pancreatic islet beta cells exhibit diabetes as a result of enhanced endoplasmic reticulum stress and apoptosis

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WFS1-deficiency increases endoplasmic reticulum stress, impairs cell cycle progression and triggers the apoptotic pathway specifically in pancreatic beta-cells

21 January 2018

1 reference

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Wolframin expression induces novel ion channel activity in endoplasmic reticulum membranes and increases intracellular calcium

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Rapid changes of mitochondrial Ca2+ revealed by specifically targeted recombinant aequorin

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Reduced loading of intracellular Ca(2+) stores and downregulation of capacitative Ca(2+) influx in Bcl-2-overexpressing cells.

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Bcl-2 decreases the free Ca2+ concentration within the endoplasmic reticulum

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Presenilin mutations linked to familial Alzheimer's disease reduce endoplasmic reticulum and Golgi apparatus calcium levels.

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BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis

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Endoplasmic reticulum Ca(2+) homeostasis and neuronal death.

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Monitoring dynamic changes in free Ca2+ concentration in the endoplasmic reticulum of intact cells

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