Browse our anti-APH1A (APH1A) Antibodies

Mouse (Murine) Anterior Pharynx Defective 1 Homolog A (C. Elegans) (APH1A) interaction partners

1. Prostaglandin I2 accumulation in neuronal cells activates PKA/CREB (show CREB1 Antibodies) and JNK/c-Jun signaling pathways by phosphorylation, which results in APH-1alpha/1beta expression.

2. Thus, Leda-1/Pianp (show C12orf53 Antibodies) is constitutively processed by proprotein convertases, sheddases including MMPs and ADAM10 (show ADAM10 Antibodies)/17 and intramembrane protease gamma-secretase.

3. Abeta (show APP Antibodies) oligomers in the cerebrospinal fluid (CSF (show CSF2 Antibodies)) further promoted the expression of APH-1alpha/-1beta (by >2.5-fold), which enhances the gamma-cleavage of APP (show APP Antibodies) and Abeta (show APP Antibodies) deposition during AD progression

4. Upregulation of PS1 (show PSEN1 Antibodies)/gamma-secretase activity may be a risk factor for late onset sporadic Alzheimer's disease.

5. ficiency of beta-arrestin1 (show ARRB1 Antibodies) or inhibition of binding of beta-arrestin1 (show ARRB1 Antibodies) with APH-1 by small peptides reduced Abeta (show APP Antibodies) production without affecting Notch (show NOTCH1 Antibodies) processing

6. Pen-2 (show PSENEN Antibodies), as well as nicastrin (show NCSTN Antibodies) and Aph-1alpha, is dispensable for presenilin endoproteolysis

7. We propose a model that identifies critical TMDs of Aph-1 for associations with Nct (show NCSTN Antibodies) and PS for the stepwise assembly of gamma-secretase components.

8. Aph-1 associates directly with full-length and C-terminal fragments of gamma-secretase substrates

9. presenilin 1 (PS1 (show PSEN1 Antibodies))-derived fragments, mature nicastrin (show NCSTN Antibodies), APH-1, and PEN-2 (show PSENEN Antibodies), associate with cholesterol-rich detergent insoluble membrane (DIM) domains of non-neuronal cells and neurons

10. Our findings establish that APH-1a is the major mammalian APH-1 homolog present in presenilin-dependent gamma-secretase complexes during embryogenesis.

Human Anterior Pharynx Defective 1 Homolog A (C. Elegans) (APH1A) interaction partners

1. Using purified PSEN1 (show PSEN1 Antibodies)/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 (show APP Antibodies); present a unifying model for how PSEN (show PSEN1 Antibodies) or APP (show APP Antibodies) mutations enhance amyloidogenic Abeta (show APP Antibodies) production, suggests that environmental factors may increase Alzheimer's Disease risk.

2. Data show that presenilin 1 (PS1 (show PSEN1 Antibodies))/anterior-pharynx-defective protein 1 (Aph1b), presenilin 2 (PS2 (show PSEN2 Antibodies))/Aph1aL, PS2 (show PSEN2 Antibodies)/Aph1aS and PS2 (show PSEN2 Antibodies)/anterior pharynx defective 1 homolog B (Aph1b) gamma-secretase produced amyloid beta peptide (Abeta (show APP Antibodies)) with a higher Abeta42+Abeta43-to-Abeta40 (Abeta42(43)/Abeta40) ratio than the other gamma-secretases.

3. Data show that presenilin 1 (PS1 (show PSEN1 Antibodies))-containing gamma-secretase complexes were targeted to the plasma membrane, whereas presenilin 2 (PS2 (show PSEN2 Antibodies))-containing ones were addressed to the trans-Golgi network, to recycling endosomes.

4. No statistically significant difference was detected either in APOE (show APOE Antibodies) or APH-1a polymorphisms, not suggesting a strong susceptibility to the development of Alzheimer disease.

5. analysis of how the conformation of presenilin, Pen-2 (show PSENEN Antibodies), Aph-1, and nicastrin (show NCSTN Antibodies) affect the function and mechanism of gamma-secretase

6. We demonstrate that extending the transmembrane domain of the amyloid precursor protein (show APP Antibodies)-derived C99 substrate in proximity to the cytosolic face strongly influences gamma-secretase cleavage specificity.

7. The -980C/G polymorphism in APH-1A promoter confers risk of Alzheimer's disease

8. Coexpression of wild-type or S-palmitoylation-deficient APH1aL and nicastrin (show NCSTN Antibodies) leads to marked stabilization of transgenic presenilin 1 (show PSEN1 Antibodies) in the brains of double-transgenic mice.

9. Endogenous Aph-1a and its proteolytic fragment have unique properties for cleavage control that may have implications for gamma-secretase regulation and intracellular distribution.

10. Co-overexpression of presenilin-1 (show PSEN1 Antibodies) or APH-1 abrogated gamma-secretase inhibition probably through prevention of the incorporation of CRB2 (show CRB2 Antibodies) into the gamma-secretase complex