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Literature summary for 2.7.1.153 extracted from

  • Arancibia, S.; Beni­tez, D.; Nunez, L.; Jewell, C.; Langjahr, P.; Candia, E.; Zapata-Torres, G.; Cidlowski, J.; Gonzalez, M.; Hermoso, M.
    Phosphatidylinositol 3-kinase interacts with the glucocorticoid receptor upon TLR2 activation (2011), J. Cell. Mol. Med., 15, 339-349.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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General Information

General Information Comment Organism
physiological function phosphatidylinositol 3-kinase is critical for the TLR2 downstream effects of glucocorticoids. Cells expressing a phosphatidylinositol 3-kinase p85 subunit deletion mutant and exposed to Pam3-Cys-Ser-Lys4 in the presence or absence of dexamethasone, show enhanced tumour necrosis factor TNFalpha expression while AP-1 and NF-kappaB transcriptional activity are repressed. Phosphatidylinositol 3-kinase physically interacts with the glucocorticoid receptor through two putative phosphatidylinositol 3-kinase recruitment consensus YxxM binding motifs in the glucocorticoid receptor. The phosphatidylinositol 3-kinase-glucocorticoid receptor interaction may contribute to the effects of glucocorticoids on the TLR2 pro-inflammatory signalling cascade Homo sapiens