Titlebook: Notch from Neurodevelopment to Neurodegeneration: Keeping the Fate; Yves Christen,Alain Isra?l,Frédéric Checler Conference proceedings 200

爭(zhēng)吵加

,New Non-Peptidic Inhibitors of γ-Secretase Abolish Aβ Production Without Modifying Notch Cleavage,lytic activities responsible for the release of the N- and C-termini of Aβ peptides, respectively (for review, see .). A consensus now exists concerning β-secretase, a novel type of membrane-bound aspartyl protease recently discovered by several teams and referred to as BACE1 (β-site APP-cleaving en

Diastole

允許

Missorting of the Dendritic Cell Adhesion Molecule Telencephalin in Presenilin-Deficient Neurons,ch intracellular domain. The presenilins are therefore implicated in such diverse processes as the neurodegeneration in Alzheimer’s disease and the regulation of Notch signaling. The question remains whether other type I transmembrane proteins or pathways are subject to presenilin-mediated proteolys

發(fā)酵劑

,βAPP Processing, its Biology and Alzheimer’s Disease, Protein (APP) by two sequential proteolytic events. Although APP proteolysis has been extensively studied because of its relevance to AD, its biologic function remains enigmatic. In this paper I propose a model in which processing of APP, under control of presenilins, generates an intracellular pep

LATHE

季雨

,PS1 Interacts With and Facilitates β-Catenin Turnover,’s disease (AD). Presenilins are polytopic membrane proteins that are predicted to span the membrane six to eight times (reviewed in .). The mechanisms by which the mutations cause early onset AD are unknown. The prevailing hypothesis centers on altered γ-secretase activity that generates the C-term

刻苦讀書(shū)

,δ-Catenin, Presenilin, and the Synaptic-Adherens Junction Complex, in the Armadillo (Arm) repeat superfamily with sequence similarity to the adherens junction protein p120.. δ-Catenin can be immunoprecipitated as a complex with other components of the adherens junction, including cadherin and β-catenin, from transfected cells and brain. The ectopic expression of δ

Euphonious

Vascular Smooth Muscle Cells Are the Primary Target of the Events Leading from Notch3 Mutations to atter lesions and diffuse alterations of the small cerebral arteries characterized by major alterations of vascular smooth muscle cells, which ultimately disappear. We recently established that CADASIL is due to mutations in the Notch3 gene..Precise mechanisms that lead from Notch3 mutations to the

spinal-stenosis

Notch Signaling in the Brain: More than Just a Developmental Story,udies have shown that elucidating the mechanism of Notch signaling and its role in the brain is important for our understanding of adult-onset neurological disorders, such as the presenilinlinked form of Alzheimer’s disease (AD) and cerebral arteriopathy CADASIL. Here we present an overview of Notch

FATAL

Control of Notch Activity by the Ubiquitin-Proteasome Pathway,ecule could stabilize intracellular Notch 1 and enhance its transcriptional activity, but had no effect on inactive, membrane-anchored forms of the receptor. We then demonstrated that SEL-10 specifically interacts with nuclear forms of Notchl and that this interaction requires a phosphorylation even