The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-α/β-mediated apoptosis in Ubp43-deficient hematopoietic cells
Copyright policy )The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-α/β-mediated apoptosis in Ubp43-deficient hematopoietic cells
UBP43 (also known as USP18) plays a role in the negative regulation of interferon-α/β signaling, and bone marrow cells in Ubp43-deficient mice exhibited hypersensitivity to interferon-α/β-mediated apoptosis. Here, we show that the mitochondrial apoptotic pathway and reactive oxygen species are major contributors to the elevated interferon-α/β-mediated apoptosis in Ubp43-deficient mouse bone marrow cells and in UBP43-knockdown THP-1 cells. Furthermore, TRAIL and FASL, which were proposed as apoptosis inducers upon interferon-α/β treatment in UBP43-knockdown adherent cancer cells, did not cause apoptosis in these hematopoietic cells. Therefore, although UBP43 depletion can cause hypersensitivity to interferon-α/β-mediated apoptosis in a broad range of cell types, the downstream pathway may vary depending on the cell type.
- Sookmyung Women's University Korea (Republic of)
- University of California, San Diego United States
- University of California, San Diego United States
- Moores Cancer Center United States
- UC San Diego Health System United States
Fas Ligand Protein, Caspase 3, Interferon-alpha, Apoptosis, Interferon-beta, Hematopoietic Stem Cells, Cell Line, Mitochondria, TNF-Related Apoptosis-Inducing Ligand, Mice, Cell Line, Tumor, Gene Knockdown Techniques, Endopeptidases, Animals, Humans, Reactive Oxygen Species, Ubiquitin Thiolesterase, Metabolic Networks and Pathways
Fas Ligand Protein, Caspase 3, Interferon-alpha, Apoptosis, Interferon-beta, Hematopoietic Stem Cells, Cell Line, Mitochondria, TNF-Related Apoptosis-Inducing Ligand, Mice, Cell Line, Tumor, Gene Knockdown Techniques, Endopeptidases, Animals, Humans, Reactive Oxygen Species, Ubiquitin Thiolesterase, Metabolic Networks and Pathways
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