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http://dx.doi.org/10.4014/jmb.1503.03088

Histone H3 is Digested by Granzyme A During Compromised Cell Death in the Raji Cells  

Lee, Phil Young (Functional Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Park, Byoung Chul (Functional Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Chi, Seung Wook (Functional Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Bae, Kwang-Hee (Functional Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Kim, Sunhong (Incurable Diseases Therapeutics Reasearch Center, Korea ResearchInstitute of Bioscience & Biotechnology (KRIBB))
Cho, Sayeon (College of Pharmacy, Chung-Ang University)
Kim, Jeong-Hoon (Epigenomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Park, Sung Goo (Functional Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB))
Publication Information
Journal of Microbiology and Biotechnology / v.25, no.9, 2015 , pp. 1578-1582 More about this Journal
Abstract
Granzyme A (GzmA) was identified as a cytotoxic T lymphocyte protease protein expressed in the nucleus. A number of nuclear proteins are well known as GzmA substrates, and GzmA is related with caspase-independent apoptosis. Histones H1, H2B, and H3 were identified as GzmA substrates through in vitro experiment with purified nucleosome. Here, we demonstrated that histone H3 was cleaved by GzmA in vivo during staurosporine-induced cell death. Moreover, histone H3 cleavage was blocked by the GzmA inhibitor nafamostat mesylate and by GzmA knockdown using siRNA. Taken together, we verified that histone H3 is a real substrate for GzmA in vivo in the Raji cells treated by staurosporin.
Keywords
Caspase-independent cell death; histone H3; granzyme A;
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