1. Catalog
  2. Nodes
  3. p(HGNC:APP, pmod(Ph, Thr, 668))

p(HGNC:APP, pmod(Ph, Thr, 668))

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

Entity

Name
APP
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 3

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

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Protein phosphatase 2A dysfunction in Alzheimer’s disease v1.0.0

In-Edges 4

p(HGNC:APP) hasVariant p(HGNC:APP, pmod(Ph, Thr, 668)) View Subject | View Object

Appears in Networks:

complex(p(HBP:HBP00071), p(HGNC:MAPK8IP1)) regulates p(HGNC:APP, pmod(Ph, Thr, 668)) View Subject | View Object

By binding to AICD, JIP mediates APP/AICD phosphorylation at Thr668, thus modulating APP trafficking, maturation and processing PubMed:22122372

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons

act(p(HGNC:DAPK1), ma(kin)) increases p(HGNC:APP, pmod(Ph, Thr, 668)) View Subject | View Object

Furthermore, DAPK1-induced APP phosphorylation was suppressed when DAPK1 ΔDD was introduced (Fig. 4G), indicating that DAPK1 regulates Aβ secretion through APP Thr668 phosphorylation. PubMed:27094130

Appears in Networks:

bp(GO:"one-carbon metabolic process") decreases p(HGNC:APP, pmod(Ph, Thr, 668)) View Subject | View Object

Remarkably, impairment of one-carbon metabolism in animal models can reproduce AD-like pathological features: accumulation of P-tau (Sontag et al.,2007; Zhang et al.,2008; Wei et al.,2011); enhanced amyloidogenesis (Pacheco-Quinto et al.,2006; Zhang et al.,2009; Zhuo et al.,2010; Zhuo and Pratico,2010); increased phosphorylation of APP at the regulatory Thr-668 site (Sontag et al.,2007; Zhang et al.,2009); increased sensitivity to amyloid toxicity (Kruman et al.,2002); and cognitive impairment (Bernardo et al.,2007; Wei et al.,2011; Rhodehouse et al., 2013). PubMed:24653673

Appears in Networks:

Out-Edges 2

p(HGNC:APP, pmod(Ph, Thr, 668)) regulates sec(p(HGNC:APP, frag("672_711"))) View Subject | View Object

Furthermore, DAPK1-induced APP phosphorylation was suppressed when DAPK1 ΔDD was introduced (Fig. 4G), indicating that DAPK1 regulates Aβ secretion through APP Thr668 phosphorylation. PubMed:27094130

Appears in Networks:

p(HGNC:APP, pmod(Ph, Thr, 668)) regulates sec(p(HGNC:APP, frag("672_713"))) View Subject | View Object

Furthermore, DAPK1-induced APP phosphorylation was suppressed when DAPK1 ΔDD was introduced (Fig. 4G), indicating that DAPK1 regulates Aβ secretion through APP Thr668 phosphorylation. PubMed:27094130

Appears in Networks:

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.