Functional Myc-Max heterodimer is required for activation-induced apoptosis in T cell hybridomas.
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TLDR
It is shown that coexpression of a reciprocally mutant Myc protein capable of forming functional heterodimers with the mutant Max can compensate for the dominant negative activity and restore activation-induced apoptosis.Abstract:
T cell hybridomas respond to activation signals by undergoing apoptotic cell death, and this is likely to represent comparable events related to tolerance induction in immature and mature T cells in vivo. Previous studies using antisense oligonucleotides implicated the c-Myc protein in the phenomenon of activation-induced apoptosis. This role for c-Myc in apoptosis is now confirmed in studies using a dominant negative form of its heterodimeric binding partner, Max, which we show here inhibits activation-induced apoptosis. Further, coexpression of a reciprocally mutant Myc protein capable of forming functional heterodimers with the mutant Max can compensate for the dominant negative activity and restore activation-induced apoptosis. These results imply that Myc promotes activation-induced apoptosis by obligatory heterodimerization with Max, and therefore, by regulating gene transcription.read more
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Lymphocyte apoptosis and apoptosis-associated gene expression in Sjögren's syndrome
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c-Myc does not prevent glucocorticoid-induced apoptosis of human leukemic lymphoblasts.
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MXD3 as an onco-immunological biomarker encompassing the tumor microenvironment, disease staging, prognoses, and therapeutic responses in multiple cancer types
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Molecular cloning and chromosomal mapping of mouse intronless myc gene acting as a potent apoptosis inducer
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References
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Journal Article
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TL;DR: This highly reproducible, quantitative assay for T cell growth factor (TCGF), based upon the tritiated-thymidine incorporation of continuous murine tumor-specific cytotoxic T cell lines (CTLL), has revealed that T lymphocytes are required for its production.
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TL;DR: The present review describes several methods to characterize and differentiate between two different mechanisms of cell death, apoptosis and necrosis, applied to studies of apoptosis triggered in the human leukemic HL-60 cell line by DNA topoisomerase I or II inhibitors, and in rat thymocytes by either topoisomersase inhibitors or prednisolone.
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