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Specific phosphorylation of αA‐crystallin is required for the αA‐crystallin‐induced protection of astrocytes against staurosporine and C2‐ceramide toxicity
Author(s) -
Georg Reiser,
Li Rongyu
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb183
Subject(s) - staurosporine , crystallin , phosphorylation , ceramide , microbiology and biotechnology , cytoprotection , downregulation and upregulation , p38 mitogen activated protein kinases , protein kinase a , kinase , biology , neurodegeneration , mapk/erk pathway , chemistry , protein kinase c , biochemistry , oxidative stress , apoptosis , medicine , gene , disease
a‐Crystallin is upregulated in neurodegenerative diseases and neurodegenerative conditions. Elevated a‐crystallin apparently plays a self‐protective function. Compared to the studies on the expression and role of aB‐crystallin in the nervous system, there are considerably fewer reports on the role of aA‐crystallin in the brain. We reported that aA‐crystallin and protease‐activated receptor are involved in protection of astrocytes against C2‐ ceramide‐ and staurosporine‐induced cell death (Li et al., J Neurochem 110, 2009, 1433–1444). We investigated the molecular mechanism of aA‐crystallin‐mediated cytoprotection. The phosphorylation of aA‐crystallin at Ser122 and Ser148 is required for protection. We proved that phosphorylation of aB‐crystallin at Ser45 and Ser59 is required for protection. ERK and p38 mediated the protective process by aB‐crystallin.