(Q46527301)

22 December 2017

title

Conditional inactivation of nicastrin restricts amyloid deposition in an Alzheimer's disease mouse model (English)

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22 December 2017

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GOA release 2020-03-11

author name string

Katia Sesele

1

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22 December 2017

Kalliopi Thanopoulou

2

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22 December 2017

Evi Paouri

3

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22 December 2017

Eliona Tsefou

4

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22 December 2017

Apostolos Klinakis

5

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22 December 2017

Spiros Georgopoulos

6

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22 December 2017

publication date

11 August 2013

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22 December 2017

published in

Aging Cell

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22 December 2017

volume

12

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22 December 2017

issue

6

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22 December 2017

page(s)

1032-1040

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22 December 2017

Activation and intrinsic gamma-secretase activity of presenilin 1.

cites work

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

A CamKIIalpha iCre BAC allows brain-specific gene inactivation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Nicastrin is required for Presenilin-mediated transmembrane cleavage in Drosophila

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Aph-1, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Presenilin and nicastrin regulate each other and determine amyloid beta-peptide production via complex formation

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Nicastrin is dispensable for gamma-secretase protease activity in the presence of specific presenilin mutations

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

APH-1 interacts with mature and immature forms of presenilins and nicastrin and may play a role in maturation of presenilin.nicastrin complexes

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Cortical dysplasia resembling human type 2 lissencephaly in mice lacking all three APP family members

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Presenilin-1 affects trafficking and processing of betaAPP and is targeted in a complex with nicastrin to the plasma membrane

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Lack of LDL receptor enhances amyloid deposition and decreases glial response in an Alzheimer's disease mouse model

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Overexpression of low-density lipoprotein receptor in the brain markedly inhibits amyloid deposition and increases extracellular A beta clearance

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

γ-Secretase is a membrane protein complex comprised of presenilin, nicastrin, aph-1, and pen-2

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Aph-2/Nicastrin: an essential component of gamma-secretase and regulator of Notch signaling and Presenilin localization

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Positive and negative regulation of the gamma-secretase activity by nicastrin in a murine model

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

A toolbox of Cre-dependent optogenetic transgenic mice for light-induced activation and silencing

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Loss of nicastrin elicits an apoptotic phenotype in mouse embryos.

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice.

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Deciphering Alzheimer disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Nicastrin functions as a gamma-secretase-substrate receptor

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Intramembrane proteolysis by gamma-secretase

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Conditional forebrain inactivation of nicastrin causes progressive memory impairment and age-related neurodegeneration

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Contribution of the γ-secretase subunits to the formation of catalytic pore of presenilin 1 protein

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

γ-Secretase inhibitors and modulators for Alzheimer's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Nicastrin modulates presenilin-mediated notch/glp-1 signal transduction and betaAPP processing

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

APP processing and synaptic plasticity in presenilin-1 conditional knockout mice

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Identification of a tetratricopeptide repeat-like domain in the nicastrin subunit of γ-secretase using synthetic antibodies

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

Gamma-secretase composed of PS1/Pen2/Aph1a can cleave notch and amyloid precursor protein in the absence of nicastrin

21 January 2018

1 reference

https://api.crossref.org/works/10.1111%2FACEL.12131

21 January 2018

Identifiers

DOI

10.1111/ACEL.12131

1 reference

22 December 2017

PubMed ID

23826707

1 reference

22 December 2017