Table 1.

Cellular models of p66shc inactivation (via either p66shc gene deletion or expression of а dominant-negative mutant of p66shc at S36) with phenotype of apoptosis resistance

Cells	Cell line name	Organism	Apoptosis inducer	References
Embryonic fibroblasts	MEF	mouse	H2O2, UV, staurosporine, isothiocyanate, chloroform	[2, 15, 17, 18]
Primary cardiomyocyte		mouse	angiotensin II	[19]
Transformed renal epithelial cells	TKPTS	mouse	H2O2, cisplatin	[13]
Hepatocytes transgenic for human TGFa	AML12	mouse	hypoxia-reoxygenation	[20]
Endothelial progenitor cells	BM c-kit+	mouse	high glucose in media	[21]
Osteoblastic cells	OB-6, UAMS-32	mouse	H2O2	[22]
Pheochromocytoma	PC12	rat	beta amyloid, constitutively active Rac1 mutant	[23]
Cardiomyocyte	ARVM	rat	high glucose in media	[24]
Transformed fibroblast-like cells	COS7	green monkey	constitutively active Rac1 mutant	[25]
Neuroblastoma	SH-SY5Y	human	beta amyloid	[23]
Human podocytes immortalized with SV40-T-antigen	CIDHPs	human	HIV-1 transfection	[26]
Prostatic carcinoma	PC3, LNCaP	human	isothiocyanate	[18]
Cervical carcinoma	HeLa	human	H2O2	[27]
Osteosarcoma	SaOs-2	human	H2O2	[27]
Retinal pigmented epithelial Cells	RPE	human	H2O2	[28]
Lymphoma	Jurcat	human	hypoxia, calcium ionophores	[29]
Transformed renal epithelial cells	φNx-293	human	cell detachment from a solid matrix	[30]
Endothelial cells	HuVec	human	cell detachment from a solid matrix	[30]