Table 3. Gene-targeted mouse models of Class I PI3K.

Class I PI3K	Genotype	Phenotypes	References
p110 α	p110 α -/-	Embryonic lethality (E10.5)	92
	p110 α D933A/D933A	Embryonic lethality (E10.5) E10-11; severe vascular abnormalities at E10.5	97, 98
	p110 α +/D933A	Defective in growth and metabolic regulation associated with hyperinsulinemia and glucose intolerance	98
	p110 α RBD/RBD	Defective lymphatic development ; a small fraction survived into adult associated with proliferative defects and altered growth factor signaling to PI3K; protected from Kras-driven tumorigenesis in a lung cancer model	126
	Endothelial p110 α -/-	Severe vascular abnormalities at E10.5 and died before E12.5	97
	Prostate p110 α -/-	Normal for prostate development; not protected from PTEN-loss induced high grade PIN	93
p110β	p110 β -/-	Embryonic lethality (E3.5)	91
	p110 β K805R/K805R	Some survived to adult associated with retarded growth and mild insulin resistance with age; attenuated Erbb2-driven mammary tumor development	95
	Liver p110 β -/-	Impaired insulin sensitivity and glucose homeostasis	93
	Prostate p110 β -/-	Normal for prostate development; protected from PTEN-loss induced high grade PIN	93
p110δ	p110 $\stackrel{\sim }{\delta }$	Viable; impaired B, NK cell development and functions; decreased immunoglobulin levels and defective humoral response; impaired neutrophil chemotaxis	180-186
	p110 δ D910A/D910A	Viable; defective B, NK and mast cell development and function; impaired antigen receptor signaling in B and T cells, and attenuated immune and allergic response	180-186
p110γ	p110 $\stackrel{\sim }{\gamma }$	Viable; reduced insulin secretion; increased insulin sensitivity and β-cell mass; impaired mast cell functions and inflammatory response; reduced neutrophil and macrophage migration and oxidative burst; increased heart contractility	10, 187-192
	p110 γ KD/KD	Viable; reduced inflammatory reactions with no alterations in cardiac contractility	9
	p110 $\stackrel{\sim }{\delta }$ p110 $\stackrel{\sim }{\gamma }$	Viable; severe defects in T and NK cell development and functions	193-195
p85	p85 α -/-	Hypoglycemia and hypoinsulinemia and impaired B cell development and functions but normal T cell activation	196, 197
	p55 α -/-p50 α -/-	Viable; enhanced insulin sensitivity	198
	p85 α -/- p55 α -/-p50 α -/-	Perinatal death; liver necrosis and hypoglycemia; increased insulin sensitivity; impaired B cell development and functions	199, 200
	p85 β -/-	Improved insulin sensitivity, increased T cell proliferation and accumulation in response to various stimuli	201
	Liver p85 α -/- p55 α -/-p50 α -/- p85 β -/-	Defects in glucose and lipid homeostatis; hyperinsulinemia and hypolipidemia	202
	Muscle α -/- p55 α -/-p50 α -/- p85 β -/-	Viable; reduced muscle growth, insulin response, and hyperlipidemia	203
	Endothelial p85 α -/- p55 α -/-p50 α -/- p85 β -/-	Acute embryonic lethality at E11.5 due to hemorrhaging	129
	Endothelial p85 α +/- p55 α -/-p50 α -/- p85 β -/-	Viable but with localized vascular abnormalities when challenged with pathlogical insults	129