p110δ Phosphoinositide 3-Kinase Represses IgE Switch by Potentiating BCL6 Expression

p110δ phosphoinositide 3-kinase represses IgE switch by potentiating BCL6 expression.

PI3Ks are key signaling enzymes required for triggering many immunological functions. In B lymphocytes, PI3K signaling is required for Ag-induced proliferation and robust production of most Ab isotypes. Paradoxically, PI3K was found to have a negatively regulatory function regarding Ab class switch recombination, and blockade of PI3K can strongly potentiate IgE switch. In this article, we explo...

p110d Phosphoinositide 3-Kinase Represses IgE Switch by Potentiating BCL6 Expression

Expression of the phosphoinositide 3-kinase p110δ isoform and its clinicopathological significance in gastric cancer

Protein p110δ is an isoform of the catalytic subunit of class I phosphoinositide 3-kinases (PI3Ks). PI3Ks are involved in the regulation of cell survival, growth, proliferation, and migration, and have been implicated in the oncogenesis of hematologic malignancies. In this study, we evaluated the expression of p110δ in gastric cancer (GC) and its association with various clinicopathological fac...

Regulation of p110δ PI 3-Kinase Gene Expression

BACKGROUND Despite an intense interest in the biological functions of the phosphoinositide 3-kinase (PI3K) signalling enzymes, little is known about the regulation of PI3K gene expression. This also applies to the leukocyte-enriched p110delta catalytic subunit of PI3K, an enzyme that has attracted widespread interest because of its role in immunity and allergy. PRINCIPAL FINDINGS We show that...

Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling.

Insulin plays a key role in regulating a wide range of cellular processes. However, until recently little was known about the signalling pathways that are involved in linking the insulin receptor with downstream responses. It is now apparent that the activation of class 1a phosphoinositide 3-kinase (PI 3-kinase) is necessary and in some cases sufficient to elicit many of insulin's effects on gl...