Akt/PKB signaling pathway: Difference between revisions
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=Activation Akt/PKB via Receptor tyrosine kinases/Ras= | =Activation Akt/PKB via Receptor tyrosine kinases/Ras= | ||
==[[Receptor tyrosine kinases]]== | ==[[Receptor tyrosine kinases]]== | ||
==[[Growth factor receptor-bound proteins]]== | |||
==Ras activation== | ==Ras activation== | ||
[[GTPase KRas]] | [[GTPase KRas]] | ||
[[Allosteric modulation of H-Ras GTPase]] | [[Allosteric modulation of H-Ras GTPase]] | ||
=Phosphoinositide 3-Kinases= | |||
Phosphoinositide 3-Kinases or phosphatidylinositol 3-kinase (PI3K) are a family of ubiquitously distributed lipid kinases, that play a critical role in the regulation of numerous cellular processes including cellular growth and morphology, programmed cell death, cell motility and adhesion, mitogenesis and glucose uptake. | |||
*[[The Structure of PI3K]] | |||
*[[Phosphoinositide 3-Kinases]] | |||
*[[PI3K Activation, Inhibition, & Medical Implications]] | |||
PI3K can also be activated by [[G protein-coupled receptors]] (GPCRs), via G-protein βγ dimers or Ras which bind PI3K directly. In addition, the Gα subunit activates Src-dependent integrin signaling which can activate PI3K. | |||
==Phosphoinositide formation== | |||
The triphosphate form (PI(3,4,5)P3) binds Akt and [[phosphoinositide-dependent kinase 1]] (PDK1) so they accumulate in close proximity at the membrane. | |||
=Akt/PKB= | =Akt/PKB= | ||