| Interaction ID | Mol A | Type | Species | Verb | Nature | Mol B | Type | Species |   |
|---|
|
| 117732 | BACE1 | Protein | Homo sapiens-e | Increases pro-cleavage | direct | APP | Protein | Homo sapiens-e | | | Caveolin-3 upregulation activates
beta-secretase-mediated cleavage of the amyloid precursor
protein in Alzheimer's disease. / In addition, we find
that caveolin-3 physically interacts and biochemically
colocalizes with amyloid precursor protein (APP) both in
vivo and in vitro. Interestingly, recombinant overexpression
of caveolin-3 in cultured cells stimulated
beta-secretase-mediated processing of APP. | | | |
Interaction id | 117732 | |
MOLECULE A | |
Id | 23621 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | -- | |
MOLECULE B | |
Id | 351 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | | Kinetics | - | |
|
General Information |
Interaction term | Increases pro-cleavage (
direct ) | |
Pathway | | |
Disease Details | | disease: :Alzheimer Disease |
| |
Experimental location and method | - condition::Cultured astroglial cells
from authentic AD patients
| |
References | |
PubMed Id | 10414982 | |
Author | Nishiyama K, Trapp BD, Ikezu T, Ransohoff RM, Tomita T,
Iwatsubo T, Kanazawa I, Hsiao KK, Lisanti MP, Okamoto T | |
Title | Caveolin-3 upregulation activates beta-secretase-mediated
cleavage of the amyloid precursor protein in Alzheimer's disease. |
|
|
| | |
| 215029 | PPARG | Protein | Homo sapiens-e | Decreases activity | direct | BACE1 | DNA | Homo sapiens-e | | | Nonsteroidal anti-inflammatory drugs repress
beta-secretase gene promoter activity by the activation of
PPARgamma. / Conversely, overexpression of PPARgamma, as
well as NSAIDs and PPARgamma activators, reduced BACE1 gene
promoter activity. These results suggested that PPARgamma
could be a repressor of BACE1. We then identified a
PPARgamma responsive element (PPRE) in the BACE1 gene
promoter. Mutagenesis of the PPRE abolished the binding of
PPARgamma to the PPRE and increased BACE1 gene promoter
activity. / Interestingly, brain extracts from AD patients
showed decreased PPARgamma expression and binding to PPRE in
the BACE1 gene promoter. | | | |
Interaction id | 215029 | |
MOLECULE A | |
Id | 5468 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | disease: :Alzheimer Diseaseexpression: :Low | |
MOLECULE B | |
Id | 23621 |
Type | DNA |
Species | Homo sapiens-e | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | |
Regulator | |
Regulation | Positive | | Description | Nonsteroidal anti-inflammatory drug |
|
| | Kinetics | - | |
|
General Information |
Interaction term | Decreases activity (
direct ) | |
Pathway | Ligand-dependent nuclear receptor
activity:Peroxisome proliferator associated receptor activity | |
Disease Details | | disease: :Alzheimer Disease |
| |
Experimental location and method | - Experimental method::Mutation analysis
| |
Comments | |
Property | | Mutated molecule:BACE1(PPARgamma responsive element) |
Domain_motif_site_residue | | [US:PPARgamma responsive element](23621) |
| |
References | |
PubMed Id | 16407166 | |
Author | Sastre M, Dewachter I, Rossner S, Bogdanovic N, Rosen E,
Borghgraef P, Evert BO, Dumitrescu-Ozimek L, Thal DR, Landreth
G, Walter J, Klockgether T, van Leuven F, Heneka MT | |
Title | Nonsteroidal anti-inflammatory drugs repress beta-secretase
gene promoter activity by the activation of PPARgamma. |
|
|
| |
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