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      Requirement for the orphan steroid receptor Nur77 in apoptosis of T-cell hybridomas.

      Nature

      Apoptosis, genetics, physiology, DNA-Binding Proteins, Hybridomas, metabolism, Mutation, Nuclear Receptor Subfamily 4, Group A, Member 1, Receptors, Cytoplasmic and Nuclear, Receptors, Steroid, T-Lymphocytes, Transcription Factors

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          Abstract

          Apoptosis is a phenomenon observed during development of many cell types in many organisms. It is an internal, programmed cell death characterized by DNA fragmentation into nucleosome-size pieces. Anti-CD3-induced apoptosis in T-cell hybridomas and immature thymocytes requires new gene transcription and may be related to negative selection during T-cell development. Using subtractive hybridization, we isolated a complementary DNA clone encoding the orphan steroid receptor Nur77 (refs 7-9). It shows different patterns of messenger RNA induction between apoptotic and stimulated T cells. We report here the use of gel shift analysis to demonstrate that the Nur77 protein is present at high levels in apoptotic T-cell hybridomas and apoptotic thymocytes, but not in growing T cells or stimulated splenocytes. A Nur77 dominant negative protected T-cell hybridomas from activation-induced apoptosis. Hence Nur77 is necessary for induced apoptosis in T-cell hybridomas.

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          Journal
          8121493
          10.1038/367277a0

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