ArticleBMB reports2016
Histone H4 is cleaved by granzyme A during staurosporine-induced cell death in B-lymphoid Raji cells.
Article in BMB reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Histone Tail Cleavage as a Mechanism for Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Emerging therapeutic strategies targeting extracellular histones for critical and inflammatory diseases: an updated narrative review.Frontiers in immunology · 2024Review
- Tracking the Dynamic Histone Methylation of H3K27 in Live Cancer Cells.ACS sensors · 2021Article
- Effect of histone H4 tail on nucleosome stability and internucleosomal interactions.Scientific reports · 2021Article
- Involvement of p53-dependent apoptosis signal in antitumor effect of Colchicine on human papilloma virus (HPV)-positive human cervical cancer cells.Bioscience reports · 2020Article
- Histone tail cleavage as a novel epigenetic regulatory mechanism for gene expression.BMB reports · 2018Review
- Reactive oxygen species-dependent apoptosis induction by water extract ofNutrition research and practice · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. [BMB Reports 2016; 49(10): 560-565].
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Registered trials
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