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HuD regulates apoptosis in N2a cells by regulating Msi2 expression.

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  • معلومة اضافية
    • المصدر:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: San Francisco, CA : Public Library of Science
    • الموضوع:
    • نبذة مختصرة :
      HuD plays a critical role in neurite outgrowth, neuronal plasticity, and survival. However, HuD autoantibodies from patients with paraneoplastic gut dysmotility can trigger the apoptotic cascade in human neuroblastoma cell line and myenteric neurons. The mechanism by which HuD regulates the apoptotic pathway is unclear. Apoptosis is one of the underlying causes of neurodegenerative diseases like Alzheimer's disease. In the current study, we found that HuD interacts with Msi2 transcript and positively regulates it in the mouse neuroblastoma (N2a) cells. MSI2 being an RNA binding protein has diverse mRNA targets and regulates the mitochondrial apoptotic pathway by interacting with and repressing APAF1 transcript. Conversely, the reduced levels of HuD leads to decreased Msi2 expression and increased APAF1 levels, which results in apoptosis in N2a cells. Overall, our research indicates that HuD and Msi2 possess an anti-apoptotic role in N2A cells.
      Competing Interests: The authors have declared that no competing interests exist.
      (Copyright: © 2024 Gaikwad et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
    • الرقم المعرف:
      0 (RNA-Binding Proteins)
      0 (ELAV-Like Protein 4)
      0 (Apoptotic Protease-Activating Factor 1)
      0 (Elavl4 protein, mouse)
      0 (RNA, Messenger)
    • الموضوع:
      Date Created: 20241216 Date Completed: 20241216 Latest Revision: 20241216
    • الموضوع:
      20241217
    • الرقم المعرف:
      10.1371/journal.pone.0315535
    • الرقم المعرف:
      39680531