Table 1.

Non-cell death related functions of anti-apoptotic proteins.

Anti-apoptotic proteins	Physiological state
BCL-2	Regulates ER Ca2+ homeostasis by decreasing the ER Ca2+ uptake (Ferrari et al., 2002; Rudner et al., 2002)
	Supports axon regeneration and neurite outgrowth (Jiao et al., 2005)
BCL-XL	Involved in synapse formation
	Increases synapse number and localization of mitochondria to synapse (Hickman et al., 2008)
	Maintains mitochondrial fusion, fission, and biomass (Berman et al., 2009)
	Stabilizes mitochondrial membrane potential by directly interacting with ATP synthase (Chen et al., 2011)
	Stabilizes IP3-receptor mediated Ca2+ signaling in astrocytes (Martorana et al., 2012)
BCL-w	Regulates neuronal excitability by modulating GABA-mediated currents (Murphy et al., 2007)
MCL-1	Localizes on mitochondrial outer membrane and inner membrane. Antagonizes anti-apoptotic proteins and maintains normal mitochondrial bioenergetics status (Perciavalle et al., 2012)
	Regulates mitochondrial fusion, fission, and cristae formation and facilitates ATP production (Perciavalle et al., 2012)
	Maintains cystosolic Ca2+ homeostasis and increases mitochondrial membrane potential (Anilkumar et al., 2013)