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Decline of DNA damage response along with myogenic differentiation

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  • معلومة اضافية
    • Contributors:
      Laboratoire de Radiobiologie des expositions accidentelles (IRSN/PSE-SANTE/SERAMED/LRAcc); Service de recherche en radiobiologie et en médecine régénérative (IRSN/PSE-SANTE/SERAMED); Institut de Radioprotection et de Sûreté Nucléaire (IRSN)-Institut de Radioprotection et de Sûreté Nucléaire (IRSN); Pathophysiologie et génétique du neurone et du muscle (PGNM); Université Claude Bernard Lyon 1 (UCBL); Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS); Laboratoire de micro-irradiation, de métrologie et de dosimétrie neutrons (IRSN/PSE-SANTE/SDOS/LMDN); Service de dosimétrie (IRSN/PSE-SANTE/SDOS); AFM-Téléthon, France (Plan stratégique MyoNeurAlp 1 and MyoNeurAlp 2); Institut National du Cancer PLBIO19-126 LS194750 INCa 2019; Ligue Contre les Cancers, France (Regional grant AURA)
    • بيانات النشر:
      HAL CCSD
      Life Science Alliance LLC
    • الموضوع:
      2023
    • Collection:
      HAL Lyon 1 (University Claude Bernard Lyon 1)
    • نبذة مختصرة :
      International audience ; DNA integrity is incessantly confronted to agents inducing DNA lesions. All organisms are equipped with a network of DNA damage response mechanisms that will repair DNA lesions and restore proper cellular activities. Despite DNA repair mechanisms have been revealed in replicating cells, still little is known about how DNA lesions are repaired in postmitotic cells. Muscle fibers are highly specialized postmitotic cells organized in syncytia and they are vulnerable to age-related degeneration and atrophy after radiotherapy treatment. We have studied the DNA repair capacity of muscle fiber nuclei and compared it with the one measured in proliferative myoblasts here. We focused on the DNA repair mechanisms that correct ionizing radiation (IR)-induced lesions, namely the base excision repair, the nonhomologous end joining, and the homologous recombination (HR). We found that in the most differentiated myogenic cells, myotubes, these DNA repair mechanisms present weakened kinetics of recruitment of DNA repair proteins to IR-damaged DNA. For base excision repair and HR, this decline can be linked to reduced steady-state levels of key proteins involved in these processes.
    • Relation:
      info:eu-repo/semantics/altIdentifier/pmid/37993260; hal-04302036; https://hal.science/hal-04302036; https://hal.science/hal-04302036v2/document; https://hal.science/hal-04302036v2/file/Decline%20of%20DNA%20damage%20response%20along%20with%20myogenic%20differentiation.pdf; PUBMED: 37993260; PUBMEDCENTRAL: PMC10665522
    • الرقم المعرف:
      10.26508/lsa.202302279
    • الدخول الالكتروني :
      https://hal.science/hal-04302036
      https://hal.science/hal-04302036v2/document
      https://hal.science/hal-04302036v2/file/Decline%20of%20DNA%20damage%20response%20along%20with%20myogenic%20differentiation.pdf
      https://doi.org/10.26508/lsa.202302279
    • Rights:
      http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess
    • الرقم المعرف:
      edsbas.6250ED9D