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Prostaglandin I2 accumulation in neuronal cells activates PKA/CREB (Montrer CREB1 Kits ELISA) and JNK/c-Jun signaling pathways by phosphorylation, which results in APH-1alpha/1beta expression.
Thus, Leda-1/Pianp is constitutively processed by proprotein convertases, sheddases including MMPs and ADAM10 (Montrer ADAM10 Kits ELISA)/17 and intramembrane protease gamma-secretase.
Abeta (Montrer APP Kits ELISA) oligomers in the cerebrospinal fluid (CSF (Montrer CSF2 Kits ELISA)) further promoted the expression of APH-1alpha/-1beta (by >2.5-fold), which enhances the gamma-cleavage of APP (Montrer APP Kits ELISA) and Abeta (Montrer APP Kits ELISA) deposition during AD progression
Upregulation of PS1 (Montrer PSEN1 Kits ELISA)/gamma-secretase activity may be a risk factor for late onset sporadic Alzheimer's disease.
ficiency of beta-arrestin1 (Montrer ARRB1 Kits ELISA) or inhibition of binding of beta-arrestin1 (Montrer ARRB1 Kits ELISA) with APH-1 by small peptides reduced Abeta (Montrer APP Kits ELISA) production without affecting Notch (Montrer NOTCH1 Kits ELISA) processing
Pen-2 (Montrer PSENEN Kits ELISA), as well as nicastrin (Montrer NCSTN Kits ELISA) and Aph-1alpha, is dispensable for presenilin endoproteolysis
We propose a model that identifies critical TMDs of Aph-1 for associations with Nct (Montrer NCSTN Kits ELISA) and PS for the stepwise assembly of gamma-secretase components.
Aph-1 associates directly with full-length and C-terminal fragments of gamma-secretase substrates
presenilin 1 (PS1 (Montrer PSEN1 Kits ELISA))-derived fragments, mature nicastrin (Montrer NCSTN Kits ELISA), APH-1, and PEN-2 (Montrer PSENEN Kits ELISA), associate with cholesterol-rich detergent insoluble membrane (DIM) domains of non-neuronal cells and neurons
Our findings establish that APH-1a is the major mammalian APH-1 homolog present in presenilin-dependent gamma-secretase complexes during embryogenesis.
Using purified PSEN1 (Montrer PSEN1 Kits ELISA)/Aph1A gamma-secretase and the APPC99-3XFLAG substrate, authors show that substrate shortening progressively destabilizes the consecutive enzyme-substrate complexes that characterize the sequential gamma-secretase processing of APP (Montrer APP Kits ELISA); present a unifying model for how PSEN (Montrer PSEN1 Kits ELISA) or APP (Montrer APP Kits ELISA) mutations enhance amyloidogenic Abeta (Montrer APP Kits ELISA) production, suggests that environmental factors may increase Alzheimer's Disease risk.
Data show that presenilin 1 (PS1 (Montrer PSEN1 Kits ELISA))/anterior-pharynx-defective protein 1 (Aph1b (Montrer aph1b Kits ELISA)), presenilin 2 (PS2 (Montrer PSEN2 Kits ELISA))/Aph1aL, PS2 (Montrer PSEN2 Kits ELISA)/Aph1aS and PS2 (Montrer PSEN2 Kits ELISA)/anterior pharynx defective 1 homolog B (Aph1b (Montrer aph1b Kits ELISA)) gamma-secretase produced amyloid beta peptide (Abeta (Montrer APP Kits ELISA)) with a higher Abeta42+Abeta43-to-Abeta40 (Abeta42(43)/Abeta40) ratio than the other gamma-secretases.
Data show that presenilin 1 (PS1 (Montrer PSEN1 Kits ELISA))-containing gamma-secretase complexes were targeted to the plasma membrane, whereas presenilin 2 (PS2 (Montrer PSEN2 Kits ELISA))-containing ones were addressed to the trans-Golgi network, to recycling endosomes.
No statistically significant difference was detected either in APOE (Montrer APOE Kits ELISA) or APH-1a polymorphisms, not suggesting a strong susceptibility to the development of Alzheimer disease.
analysis of how the conformation of presenilin, Pen-2 (Montrer PSENEN Kits ELISA), Aph-1, and nicastrin (Montrer NCSTN Kits ELISA) affect the function and mechanism of gamma-secretase
We demonstrate that extending the transmembrane domain of the amyloid precursor protein (Montrer APP Kits ELISA)-derived C99 substrate in proximity to the cytosolic face strongly influences gamma-secretase cleavage specificity.
The -980C/G polymorphism in APH-1A promoter confers risk of Alzheimer's disease
Coexpression of wild-type or S-palmitoylation-deficient APH1aL and nicastrin (Montrer NCSTN Kits ELISA) leads to marked stabilization of transgenic presenilin 1 (Montrer PSEN1 Kits ELISA) in the brains of double-transgenic mice.
Endogenous Aph-1a and its proteolytic fragment have unique properties for cleavage control that may have implications for gamma-secretase regulation and intracellular distribution.
Co-overexpression of presenilin-1 or APH-1 abrogated gamma-secretase inhibition probably through prevention of the incorporation of CRB2 into the gamma-secretase complex
This gene encodes a component of the gamma secretase complex that cleaves integral membrane proteins such as Notch receptors and beta-amyloid precursor protein. The gamma secretase complex contains this gene product, or the paralogous anterior pharynx defective 1 homolog B (APH1B), along with the presenilin, nicastrin, and presenilin enhancer-2 proteins. The precise function of this seven-transmembrane-domain protein is unknown though it is suspected of facilitating the association of nicastrin and presenilin in the gamma secretase complex as well as interacting with substrates of the gamma secretase complex prior to their proteolytic processing. Polymorphisms in a promoter region of this gene have been associated with an increased risk for developing sporadic Alzheimer's disease. Alternative splicing results in multiple protein-coding and non-protein-coding transcript variants.
gamma-secretase subunit APH-1A
, anterior pharynx defective 1 homolog A
, anterior pharynx defective 1 homolog A (C. elegans)
, N-acylaminoacyl-peptide hydrolase
, acylamino-acid-releasing enzyme-like
, presenilin-stabilization factor
, anterior pharynx defective 1a homolog