1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Apoptotic signals delivered through the T-cell receptor of a T-cell hybrid require the immediate-early gene nur77.

      Nature

      Animals, Apoptosis, drug effects, genetics, physiology, Base Sequence, DNA Primers, DNA-Binding Proteins, metabolism, Gene Expression Regulation, Hybrid Cells, Mice, Mice, Transgenic, Molecular Sequence Data, Nuclear Receptor Subfamily 4, Group A, Member 1, RNA, Messenger, Receptors, Antigen, T-Cell, Receptors, Cytoplasmic and Nuclear, Receptors, Steroid, Regulatory Sequences, Nucleic Acid, Signal Transduction, T-Lymphocytes, Thymus Gland, cytology, Transcription Factors, Transcription, Genetic, Transfection

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Engagement of the T-cell antigen receptor (TCR) on immature thymic T cells induces death by apoptosis. Although several lines of evidence indicate that apoptosis requires de novo gene expression, little is known about the molecular pathways that mediate this response. Here we show that nur77 (refs 4-7), a zinc-finger transcription factor, is expressed in response to TCR engagement in immature T cells and T-cell hybrids. Antisense inhibition of nur77 expression prevents apoptosis in TCR-stimulated cells. nur77 is also expressed in response to mitogens, but in this case transcription is regulated by 5' upstream elements that are distinct from those used for induction of apoptosis. In addition, polyadenylation is only observed on nur77 transcripts found in condemned cells. These data support a role for nur77 in cell death that may be distinct from that of activation.

          Related collections

          Author and article information

          Journal
          8121494
          10.1038/367281a0

          Comments

          Comment on this article