1. Catalog
  2. Nodes
  3. p(HGNC:CREB1, pmod(Ph))

p(HGNC:CREB1, pmod(Ph))

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

Entity

Name
CREB1
Namespace
hgnc
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/hgnc-symbols.belns

Appears in Networks 2

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

In-Edges 4

p(HGNC:CREB1) hasVariant p(HGNC:CREB1, pmod(Ph)) View Subject | View Object

Appears in Networks:

act(p(HGNC:MAPKAPK2)) increases p(HGNC:CREB1, pmod(Ph)) View Subject | View Object

The classic MAPK cascade involves activation of the small GTPase Ras, and the kinases Raf and MEK [86,87]. Downstream consequences of MAPK activation include activation of the ribosomal S6 kinases (Rsk) and the MAPK-activated protein kinase 2 (MAPKAP2), which phosphorylates several transcription factors including Elk-1 and cAMP-regulated response element binding protein (CREB) [85]. The physiological significance of this elaborate NGF-induced network remains unclear, but the sustained activation of MAPK is linked to neurotrophin-mediated neurite outgrowth [88,89] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

a(CHEBI:"2-[[7-(3,4-dimethoxyphenyl)-5-imidazo[1,2-c]pyrimidinyl]amino]-3-pyridinecarboxamide") increases p(HGNC:CREB1, pmod(Ph)) View Subject | View Object

We found that Syk inhibition with BAY61-3606 induced CREB phosphorylation, although that event is inhibited in the presence of a selective PKA inhibitor (Fig. 10, A and B) further showing that Syk inhibition results in PKA activation. PubMed:25331948

Appears in Networks:

act(p(FPLX:PKA)) increases p(HGNC:CREB1, pmod(Ph)) View Subject | View Object

We found that Syk inhibition with BAY61-3606 induced CREB phosphorylation, although that event is inhibited in the presence of a selective PKA inhibitor (Fig. 10, A and B) further showing that Syk inhibition results in PKA activation. PubMed:25331948

Appears in Networks:

Out-Edges 0

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.