Tumor Suppressor NM23-H1 Is a Granzyme A-Activated DNase during CTL-Mediated Apoptosis, and the Nucleosome Assembly Protein SET Is Its Inhibitor
摘要：
Granzyme A (GzmA) induces a caspase-independent cell death pathway characterized by single-stranded DNA nicks and other features of apoptosis. A GzmA-activated DNase (GAAD) is in an ER associated complex containing pp32 and the GzmA substrates SET, HMG-2, and Ape1. We show that GAAD is NM23-H1, a nucleoside diphosphate kinase implicated in suppression of tumor metastasis, and its specific inhibitor (IGAAD) is SET. NM23-H1 binds to SET and is released from inhibition by GzmA cleavage of SET. After GzmA loading or CTL attack, SET and NM23-H1 translocate to the nucleus and SET is degraded, allowing NM23-H1 to nick chromosomal DNA. GzmA-treated cells with silenced NM23-H1 expression are resistant to GzmA-mediated DNA damage and cytolysis, while cells overexpressing NM23-H1 are more sensitive.
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关键词：
T-Lymphocytes, Cytotoxic Hela Cells Jurkat Cells K562 Cells Nucleosomes Humans DNA-(Apurinic or Apyrimidinic Site) Lyase Monomeric GTP-Binding Proteins Deoxyribonucleases Serine Endopeptidases
DOI：
10.1016/S0092-8674(03)00150-8
被引量：
年份：
2003
Elsevier
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Elsevier
Semantic Scholar
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万方医学
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