General Information:

Id: 608
Diseases: Alzheimer disease - [OMIM]
Homo sapiens
BTO:0000007 HEK-293 cell
article
Reference: Kang DE et al.(1999) Presenilin 1 facilitates the constitutive turnover of beta-catenin: differential activity of Alzheimers disease-linked PS1 mutants in the beta-catenin-signaling pathway J. Neurosci. 19: 4229-4237 [PMID: 10341227]

Interaction Information:

Comment Both the full length and the C-terminal fragment of wild-type or familial Alzheimer disease (FAD) mutant PS1 interact with beta-catenin.
Formal Description
Interaction-ID: 3210

gene/protein

PSEN1

interacts (colocalizes) with

gene/protein

CTNNB1

Drugbank entries Show/Hide entries for CTNNB1
Comment Overexpression of PS1 led to increased association of beta-catenin with glycogen synthase kinase-3b (GSK-3b), a negative regulator of b-catenin, and accelerated the turnover of endogenous beta-catenin.
Formal Description
Interaction-ID: 3234

gene/protein

CTNNB1

interacts (colocalizes) with

gene/protein

GSK3B

if PS1 is overexpressed
Drugbank entries Show/Hide entries for CTNNB1 or GSK3B
Comment PS1 normally stimulates the degradation / turnover of beta-catenin.
Formal Description
Interaction-ID: 3246

gene/protein

PSEN1

decreases_quantity of

gene/protein

CTNNB1

Drugbank entries Show/Hide entries for CTNNB1
Comment Overexpression of PS1 led to increased association of beta-catenin with glycogen synthase kinase-3b (GSK-3b), a negative regulator of b-catenin, and accelerated the turnover of endogenous beta-catenin.
Formal Description
Interaction-ID: 9746

gene/protein

GSK3B

decreases_activity of

gene/protein

CTNNB1

(if PS1 is overexpessed) by phosphorylation of CTNNB1 that can be therefore degradated;
Drugbank entries Show/Hide entries for GSK3B or CTNNB1