PubMed:7964516 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/7964516","sourcedb":"PubMed","sourceid":"7964516","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/7964516","text":"Functional Myc-Max heterodimer is required for activation-induced apoptosis in T cell hybridomas.\nT 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 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