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Literature summary for 3.1.4.4 extracted from

  • Gadir, N.; Lee, E.; Garcia, A.; Toschi, A.; Foster, D.A.
    Suppression of TGFbeta signaling by phospholipase D (2007), Cell Cycle, 6, 2840-2845.
    View publication on PubMed
Search for more literature for 3.1.4.4

Application

Application Comment Organism
medicine suppression of TGFbeta signaling in MDA-MB-231 breast cancer cells is due to elevated acivity of phospholipase D2 and mediated by mTOR, i.e. Mammalian target of rapamycin, and by MAP kinase Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
1-butanol inhibitor of enzyme. Suppression of enzyme activity results in increased phosphorylation of Smad2 and Smad3 on sites that get phosphorylated by the TGFbeta receptor and positively regulate TGFbeta signaling and in suppression of phosphorylation on sites that are phosphorylated by MAP kinase and negatively regulate TGFbeta signaling. Suppression of enzyme activy also leads to increased expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
MDA-MB-231 cell breast cancer cell. Cells exhibit elevated enzyme activity that suppresses TGFbeta signaling. Suppression of enzyme activity or enzyme expression results in increased phosphorylation of Smad2 and Smad3 on sites that get phosphorylated by the TGFbeta receptor and positively regulate TGFbeta signaling and in suppression of phosphorylation on sites that are phosphorylated by MAP kinase and negatively regulate TGFbeta signaling. Suppression of enzyme activy also leads to increased expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 Homo sapiens
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