These results demonstrate that csynuclein can influence cell viability, signal transduction pathways and also stress response. Pro-apoptotic BAX belongs to the Bcl-2 family and plays an important role in the intrinsic apoptotic pathway through binding mitochondrial VDAC, which leads to the release of cytochrome c and finally to the initiating of apoptosis. In an elevated intraocular pressure mouse glaucoma model the expression of BAX was increased in hypertensive eyes in comparisons to control eyes. Also, a BAX deficiency in DBA/2J mouse protects RGC from cell death. The expression of BAX is regulated by transcription factor p53 which in turn is regulated by S100A4, down-regulated in c-synuclein ab treated cells. S100A4 induction in a murine non-metastatic adenocarcinoma cell line leads to an increased expression of BAX and thereby to increased apoptosis. The anti-apoptotic protein BIRC6 belongs to the inhibitor of apoptosis family and is up-regulated in c-synuclein ab treated RGC-5. BIRC6 is up-regulated in tumors and can inhibit active caspase-3. Studies show that overexpression of BIRC6 in mammalian cells inhibits apoptosis. In an ocular hypertensive glaucoma model the over-expression of BIRC4, another member of the IAP family, promotes optic nerve axon survival. VDAC 1/2/3, significantly down-regulated in this study, play an important role in apoptosis-initiation and are located on the outer mitochondrial membrane. They participate in energy balance regulation as well as in the release of pro-apoptotic factors. Studies show that a reduction of VDAC1 levels in endothelial cells attenuates endostatin induced apoptosis. Other proteins, such as active caspase-3, caspase-9 and BAD were down-regulated in this study whereas the active form of ERK called p-ERK1/2 was up-regulated in c-synuclein ab treated RGC-5. The well characterized ERK pathway transfers signals from different membrane receptors into the nucleus. It is composed of different kinases which activate ERK1. Activated ERK1, which is increased in RGC-5 treated with c-synuclein abs, is able to phosphorylate many cytoplasmic as well as nuclear targets, which leads to cell proliferation. An experimental rat glaucoma model shows that the activation of ERK leads to increased survival of rgc after ocular hypertension surgery. A MEK-ERK survival pathway is described, whereby activated MAPK participate in the phosphorylation of BAD and promote cell survival. BAD is a pro apoptotic member of the Bcl-2 family and participates in the initiation of apoptosis. Studies assume an involvement of BAD and active caspase-3 in glaucoma, which leads to the cellular protein cleavage and apoptosis. Studies show that c-synuclein is able to bind transcriptional factors and modulate the transcription of genes and factors such as JunB, MECP2, CREB1 and ATF3. Furthermore csynuclein can GSK1363089 interfere with the mitochondrial apoptosis pathway through transcriptional regulation of kinases and phosphates, which control the phosphorylation status of BAD. Other studies analyzing ab functions, such as hsp27.