Phosphoinositide 3-Kinases: Difference between revisions
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* [[Human PI3K p110alpha/p85alpha]]<br /> | * [[Human PI3K p110alpha/p85alpha]]<br /> | ||
* [[The Structure of PI3K]]<br /> | * [[The Structure of PI3K]]<br /> | ||
* [[Akt/PKB signaling pathway]]<br /> | |||
* [[Diabetes & Hypoglycemia]]. | * [[Diabetes & Hypoglycemia]]. | ||
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[[Image:PI3KTransduction.PNG|250px|left|thumb| Signal Transduction Pathway. PI3K Highlighted in Red. Click to Expand]] | [[Image:PI3KTransduction.PNG|250px|left|thumb| Signal Transduction Pathway. PI3K Highlighted in Red. Click to Expand]] | ||
{{Clear}} | {{Clear}} | ||
PI3Ks can be grouped into three distinct classes, Class I-III. Class I PI3Ks, the most well understood and thoroughly explored PI3K class, are composed of a 110kDa <scene name='Phosphoinositide_3-Kinases/Model_cat/2'>catalytic subunit</scene> and a 50-100 kDa <scene name='Phosphoinositide_3-Kinases/Model_ada/1'>adaptor subunit</scene>. Activation of Class I PI3Ks is controlled by extracellular signaling via receptors with intrinsic tyrosine kinase activity, G protein-linked receptors, or receptors coupled to [[SRC]] like protein tyrosine kinases. <ref>PMID:1851250</ref> Class II PI3Ks are relatively poorly understood but are 170-210 kDa and have in vitro substrate specificity toward PtdIns 4-P. Class III PI3Ks depend on Vps15p protein Ser/Thr kinases, which recruits the phosphatidylinositol kinase to late Golgi Compartments. <ref name="Wymann"/> | PI3Ks can be grouped into three distinct classes, Class I-III. | ||
*'''Class I PI3Ks''', the most well understood and thoroughly explored PI3K class, are composed of a 110kDa <scene name='Phosphoinositide_3-Kinases/Model_cat/2'>catalytic subunit</scene> and a 50-100 kDa <scene name='Phosphoinositide_3-Kinases/Model_ada/1'>adaptor subunit</scene>. Activation of Class I PI3Ks is controlled by extracellular signaling via receptors with intrinsic tyrosine kinase activity, G protein-linked receptors, or receptors coupled to [[SRC]] like protein tyrosine kinases. <ref>PMID:1851250</ref> | |||
*'''Class II PI3Ks''' are relatively poorly understood but are 170-210 kDa and have in vitro substrate specificity toward PtdIns 4-P. | |||
*'''Class III PI3Ks''' depend on Vps15p protein Ser/Thr kinases, which recruits the phosphatidylinositol kinase to late Golgi Compartments. <ref name="Wymann"/> | |||
===Class I Subclasses=== | ===Class I Subclasses=== | ||
PI3Ks are activated by extracellular agonists via the translocation of PI3Ks to the plasma membrane for easy access to lipid substrates. Depending on the adaptor proteins involved in the process, Class I PI3Ks are segregated into two subgroups. Those that associate with p85 will be directed to phosphorylated tyrosine motifs (Class IA), '''Phosphatidylinositol-4, 5-bisphosphate 3-kinase''' (PI3Kγ) catalyzes the conversion of 1-phosphatidyl-1D-myo-inositol-4, 5-bisphosphate and ATP to 1-phosphatidyl-1D-myo-inositol-4, 5-trisphosphate. PI3Kγ interacts with trimeric G proteins and the p101 protein (Class IB) <ref name="Wymann"/> | PI3Ks are activated by extracellular agonists via the translocation of PI3Ks to the plasma membrane for easy access to lipid substrates. Depending on the adaptor proteins involved in the process, Class I PI3Ks are segregated into two subgroups. Those that associate with p85 will be directed to phosphorylated tyrosine motifs (Class IA), '''Phosphatidylinositol-4, 5-bisphosphate 3-kinase''' (PI3Kγ) catalyzes the conversion of 1-phosphatidyl-1D-myo-inositol-4, 5-bisphosphate and ATP to 1-phosphatidyl-1D-myo-inositol-4, 5-trisphosphate. PI3Kγ interacts with trimeric G proteins and the p101 protein (Class IB) <ref name="Wymann"/> | ||
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==PI3K Activation, Inhibition, and Medical Implications== | ==PI3K Activation, Inhibition, and Medical Implications== | ||
