Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease (Q47697314)

4 February 2018

title

Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease (English)

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4 February 2018

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Guo Q

1

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4 February 2018

Fu W

2

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4 February 2018

Xie J

3

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4 February 2018

Luo H

4

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4 February 2018

Sells SF

5

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4 February 2018

Geddes JW

6

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4 February 2018

Bondada V

7

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4 February 2018

Rangnekar VM

8

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4 February 2018

Mattson MP

9

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4 February 2018

language of work or name

English

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publication date

1 August 1998

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4 February 2018

published in

Nature Medicine

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4 February 2018

volume

4

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4 February 2018

issue

8

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4 February 2018

page(s)

957-962

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4 February 2018

Expression and function of the leucine zipper protein Par-4 in apoptosis

cites work

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Immunohistochemical evidence for apoptosis in Alzheimerʼs disease

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Evidence for apoptotic cell death in Alzheimer's disease.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Apoptosis is induced by beta-amyloid in cultured central nervous system neurons

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Evidence that 4-hydroxynonenal mediates oxidative stress-induced neuronal apoptosis.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Mechanisms and genes of cellular suicide

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

The product of par-4, a gene induced during apoptosis, interacts selectively with the atypical isoforms of protein kinase C

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Caspases: the executioners of apoptosis

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Mitochondrial manganese superoxide dismutase prevents neural apoptosis and reduces ischemic brain injury: suppression of peroxynitrite production, lipid peroxidation, and mitochondrial dysfunction.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid beta-peptide: involvement of calcium and oxyradicals.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Increased Apoptosis Arising from Increased Expression of the Alzheimer's Disease–associated Presenilin-2 Mutation (N141I)

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Protein kinase C involvement in apoptosis

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Tau protein and the neurofibrillary pathology of Alzheimer's disease

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Amyloid beta-peptide and oxidative cellular injury in Alzheimer's disease

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 is linked to perturbed calcium homeostasis and enhanced oxyradical production.

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Estrogens stabilize mitochondrial function and protect neural cells against the pro-apoptotic action of mutant presenilin-1

1 reference

https://api.crossref.org/works/10.1038%2FNM0898-957

7 January 2021

Identifiers

DOI

10.1038/NM0898-957

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4 February 2018

Dimensions Publication ID

1019631043

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1 reference

4 February 2018