(Q47880180)

6 February 2018

title

Alzheimer's disease mutations in APP but not γ-secretase modulators affect epsilon-cleavage-dependent AICD production (English)

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6 February 2018

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8

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6 February 2018

Dirk Beher

object named as

Dirk Beher

10

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Patrick C Fraering

object named as

Patrick C Fraering

11

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author name string

Mitko Dimitrov

1

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6 February 2018

Jean-René Alattia

2

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6 February 2018

Thomas Lemmin

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6 February 2018

Rajwinder Lehal

4

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6 February 2018

Andrzej Fligier

5

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6 February 2018

Jemila Houacine

6

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6 February 2018

Ishrut Hussain

7

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6 February 2018

Matteo Dal Peraro

9

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6 February 2018

language of work or name

English

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publication date

1 January 2013

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6 February 2018

published in

Nature Communications

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6 February 2018

volume

4

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6 February 2018

page(s)

2246

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6 February 2018

https://scigraph.springernature.com/pub.10.1038/ncomms3246

exact match

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cites work

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

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Normal cellular processing of the beta-amyloid precursor protein results in the secretion of the amyloid beta peptide and related molecules

21 January 2018

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A presenilin-1-dependent gamma-secretase-like protease mediates release of Notch intracellular domain

21 January 2018

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Processing of the synaptic cell adhesion molecule neurexin-3beta by Alzheimer disease alpha- and gamma-secretases

21 January 2018

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Characterization of sequential N-cadherin cleavage by ADAM10 and PS1.

21 January 2018

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Phenylpiperidine-type γ-secretase modulators target the transmembrane domain 1 of presenilin 1

21 January 2018

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Substrate docking to γ-secretase allows access of γ-secretase modulators to an allosteric site

21 January 2018

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Electron microscopic structure of purified, active gamma-secretase reveals an aqueous intramembrane chamber and two pores

21 January 2018

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The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

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The Swedish mutation causes early-onset Alzheimer's disease by beta-secretase cleavage within the secretory pathway

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Potential Link between Amyloid β-Protein 42 and C-terminal Fragment γ 49–99 of β-Amyloid Precursor Protein

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Nonfibrillar diffuse amyloid deposition due to a gamma(42)-secretase site mutation points to an essential role for N-truncated A beta(42) in Alzheimer's disease

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What the halted phase III γ-secretase inhibitor trial may (or may not) be telling us.

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A subset of NSAIDs lower amyloidogenic Abeta42 independently of cyclooxygenase activity

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FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors

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The Amyloid Precursor Protein Has a Flexible Transmembrane Domain and Binds Cholesterol

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Bendix: intuitive helix geometry analysis and abstraction.

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Peptides based on the presenilin-APP binding domain inhibit APP processing and Aβ production through interfering with the APP transmembrane domain

21 January 2018

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The amyloid precursor protein and its homologues: structural and functional aspects of native and pathogenic oligomerization

21 January 2018

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Effects of membrane lipids on the activity and processivity of purified γ-secretase

21 January 2018

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Highly efficient production of the Alzheimer's γ-secretase integral membrane protease complex by a multi-gene stable integration approach

21 January 2018

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Mercury is a direct and potent γ-secretase inhibitor affecting Notch processing and development in Drosophila

21 January 2018

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21 January 2018

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21 January 2018

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21 January 2018

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21 January 2018

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Chromosome 21q21 sublocalisation of gene encoding beta-amyloid peptide in cerebral vessels and neuritic (senile) plaques of people with Alzheimer disease and Down syndrome

21 January 2018

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7 January 2021

A new pathogenic mutation in the APP gene (I716V) increases the relative proportion of A beta 42(43)

1 reference

https://api.crossref.org/works/10.1038%2FNCOMMS3246

7 January 2021

NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo

1 reference

https://api.crossref.org/works/10.1038%2FNCOMMS3246

7 January 2021

In vitro studies of amyloid beta-protein fibril assembly and toxicity provide clues to the aetiology of Flemish variant (Ala692-->Gly) Alzheimer's disease

1 reference

https://api.crossref.org/works/10.1038%2FNCOMMS3246

7 January 2021

Identifiers

DOI

10.1038/NCOMMS3246

1 reference

6 February 2018

Dimensions Publication ID

ADS bibcode

2013NatCo...4.2246D

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1000823660

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1 reference

6 February 2018