Histone H4 is cleaved by granzyme A during staurosporine-induced cell death in B-lymphoid Raji cells

被引：17

作者：

Lee, Phil Young ^{[1
,5
]}

Park, Byoung Chul ^{[1
]}

Chi, Seung Wook ^{[1
]}

Bae, Kwang-Hee ^{[2
]}

Kim, Sunhong ^{[1
]}

Cho, Sayeon ^{[4
]}

Kang, Seongman ^{[5
]}

Kim, Jeong-Hoon ^{[3
]}

Park, Sung Goo ^{[1
]}

机构：

[1] KRIBB, Dis Target Struct Res Ctr, Daejeon 34141, South Korea

[2] KRIBB, Metab Regulat Res Ctr, Daejeon 34141, South Korea

[3] KRIBB, Personalized Genom Med Res Ctr, Daejeon 34141, South Korea

[4] Chung Ang Univ, Coll Pharm, Seoul 06974, South Korea

[5] Korea Univ, Div Life Sci, Seoul 02841, South Korea

来源：

BMB REPORTS | 2016年 / 49卷 / 10期

基金：

新加坡国家研究基金会;

关键词：

Caspase-independent cell death; Granzyme A; Histone H4; Raji cell; CASPASE INHIBITORS; APOPTOSIS; NUCLEOSOME; TARGET;

D O I：

10.5483/BMBRep.2016.49.10.105

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Granzyme A (GzmA) was first identified as a cytotoxic T lymphocyte protease protein with limited tissue expression. A number of cellular proteins are known to be cleaved by GzmA, and its function is to induce apoptosis. Histones H1, H2B, and H3 were identified as GzmA substrates during apoptotic cell death. Here, we demonstrated that histone H4 was cleaved by GzmA during staurosporine-induced cell death; however, in the presence of caspase inhibitors, staurosporine-treated Raji cells underwent necroptosis instead of apoptosis. Furthermore, histone H4 cleavage was blocked by the GzmA inhibitor nafamostat mesylate and by GzmA knockdown using siRNA. These results suggest that histone H4 is a novel substrate for GzmA in staurosporine-induced cells.

引用

页码：560 / 565

页数：6

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