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p(HGNC:APBB1)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
APBB1
Namespace
hgnc
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/hgnc-symbols.belns

Appears in Networks 3

Amyloid Precursor Protein Trafficking, Processing, and Function v1.0.0

Amyloid Precursor Protein Trafficking, Processing, and Function by Thinakaran, et al., 2008

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

Proteolytic processing of Alzeimer's beta-amyloid precursor protein v1.0.1

In-Edges 4

complex(p(HGNC:APBB1), p(HGNC:APP), p(HGNC:LRP1)) hasComponent p(HGNC:APBB1) View Subject | View Object

Appears in Networks:

complex(p(HBP:HBP00071), p(HGNC:APBB1)) hasComponent p(HGNC:APBB1) View Subject | View Object

Appears in Networks:

complex(p(HBP:HBP00071), p(HGNC:APBB1), p(HGNC:KAT5)) hasComponent p(HGNC:APBB1) View Subject | View Object

Appears in Networks:

complex(p(HBP:HBP00071), p(HGNC:APBB1), p(HGNC:TFCP2)) hasComponent p(HGNC:APBB1) View Subject | View Object

Appears in Networks:

Out-Edges 4

p(HGNC:APBB1) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Overexpression of Mint1, Mint2, or Fe65 causes reduction in Aβ generation and deposition in the brains of transgenic mice, strongly suggesting a physiological role for these adaptors in regulating APP processing in the nervous tis- sue (17). PubMed:18650430

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:APBB1) decreases a(HBP:HBP00018) View Subject | View Object

Overexpression of Mint1, Mint2, or Fe65 causes reduction in Aβ generation and deposition in the brains of transgenic mice, strongly suggesting a physiological role for these adaptors in regulating APP processing in the nervous tis- sue (17). PubMed:18650430

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:APBB1) regulates bp(HBP:HBP00073) View Subject | View Object

Overexpression of Mint1, Mint2, or Fe65 causes reduction in Aβ generation and deposition in the brains of transgenic mice, strongly suggesting a physiological role for these adaptors in regulating APP processing in the nervous tis- sue (17). PubMed:18650430

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:APBB1) increases a(HBP:HBP00071) View Subject | View Object

Moreover, Fe65 stabilizes the highly labile AICD, which may serve as a regulatory step in modulating the physiological func- tion of AICD (see below). PubMed:18650430

Appears in Networks:
Annotations
Confidence
High

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.