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Entity

Name
phorbol 13-acetate 12-myristate
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 1

In-Edges 1

Out-Edges 6

a(CHEBI:"phorbol 13-acetate 12-myristate") increases act(p(FPLX:PKC)) View Subject | View Object

PMA is a known agonist of PKC, which leads to the activation of the PKC/RAS/RAF/MEK/MAPK pathway that ultimately induces NFkB activation (46–48) PubMed:25331948

a(CHEBI:"phorbol 13-acetate 12-myristate") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

PMA is a known agonist of PKC, which leads to the activation of the PKC/RAS/RAF/MEK/MAPK pathway that ultimately induces NFkB activation (46–48) PubMed:25331948

a(CHEBI:"phorbol 13-acetate 12-myristate") increases p(HGNC:RAF1, pmod(Ph)) View Subject | View Object

In particular, we monitored RAF phosphorylation following treatment with (-)-nilvadipine and observed that (-)-nilvadipine prevents RAF phosphorylation induced by PMA (Fig. 4, C and D) suggesting that (-)-nilvadipine is impacting a target upstream of RAF PubMed:25331948

a(CHEBI:"phorbol 13-acetate 12-myristate") increases p(HGNC:RAF1, pmod(Ph)) View Subject | View Object

As expected, RAF phosphorylation induced by PMA as well as basal RAF phosphorylation were reduced in 7W CHO cells transfected with SYK shRNA confirming a reduction in Syk activity (Fig. 6B). PubMed:25331948

a(CHEBI:"phorbol 13-acetate 12-myristate") increases act(p(HGNC:SYK)) View Subject | View Object

Tyrosine kinases, including Syk and Bruton’s tyrosine kinase (BTK), are activated following PMA treatment (49, 50), act upstream of RAS/RAF (51, 52), and mediate the activation of the NFkB pathway (53). PubMed:25331948

a(CHEBI:"phorbol 13-acetate 12-myristate") increases act(p(HGNC:BTK)) View Subject | View Object

Tyrosine kinases, including Syk and Bruton’s tyrosine kinase (BTK), are activated following PMA treatment (49, 50), act upstream of RAS/RAF (51, 52), and mediate the activation of the NFkB pathway (53). PubMed:25331948

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.