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Consistently, forced expression of p53 significantly stimulated ACER2 transcription. Notably, p53-mediated autophagy and apoptosis were markedly enhanced by ACER2. Depletion of the essential autophagy gene ATG5 revealed that ACER2-induced autophagy facilitates its effect on apoptosis.
Results suggest that the ACER2/sphingosine pathway mediates programmed cell death in response to DNA damage through ROS production.
c-Src-mediated signal positively regulates ACER activity in a Ca2+-independent manner.
Results suggest that up-regulation of the ACER2/DHS pathway mediates the cytotoxicity of 4-HPR in tumor cells and that up-regulating or activating ACER2 may improve the anti-cancer activity of 4-HRR and other DHC-inducing agents.
ACER2 has broad substrate specificity and requires Ca(2+) for its activity; ACER2 has the cytosolic C terminus and luminal N terminus, which are essential for its activity, correct cellular localization, and regulation for protein glycosylation
ACER2/sphingosine pathway plays an important role in regulating beta1 maturation and cell adhesion mediated by beta1 integrins
The sphingolipid metabolite sphingosine-1-phosphate promotes cell proliferation and survival, whereas its precursor, sphingosine, has the opposite effect. The ceramidase ACER2 hydrolyzes very long chain ceramides to generate sphingosine (Xu et al., 2006
alkaline ceramidase 2
, N-acylsphingosine amidohydrolase 3-like
, putative protein, with at least 4 transmembrane domains, of eukaryotic origin (5H174)
, alkCDase 2
, alkaline CDase 2
, ceramide hydrolase
, cancer related gene-liver 1 (CRG-L1)
, cancer-related gene liver 1 protein