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Erythropoietin activates caspase‐3 and downregulates CAD during erythroid differentiation in TF‐1 cells – A protection mechanism against DNA fragmentation
Author(s) -
Lui Julian Chun-Kin,
Kong Siu-Kai
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.02.059
Subject(s) - icad , dna fragmentation , apoptotic dna fragmentation , microbiology and biotechnology , fragmentation (computing) , apoptosis , caspase , biology , erythropoiesis , chemistry , biochemistry , programmed cell death , medicine , ecology , anemia
The involvement of caspase‐3 and its failure in the induction of DNA fragmentation during erythropoiesis were investigated with TF‐1 cells. During erythroid differentiation, caspase‐3 activation and cleavage of caspase‐3 substrates such as ICAD (inhibitor of caspase‐activated DNase) were detected without concomitant phosphatidyl‐serine (PS) externalization and DNA fragmentation. These observations are in contrast to our understanding that DNA is degraded by CAD (caspase‐activated DNase) when ICAD is cleaved by caspase‐3. Our study demonstrates that CAD is downregulated at the mRNA and protein level during the erythroid differentiation in TF‐1 cells. This provides a mechanism for the first time how cells avoid DNA fragmentation with activated caspase‐3.