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Heat shock-induced dissociation of TRF2 from telomeres does not initiate a telomere-dependent DNA damage response

Authors

  • Nadezhda V. Petrova,

    1. Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia
    2. Department of Molecular Biology, Lomonosov Moscow State University, Moscow, Russia
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  • Artem K. Velichko,

    1. Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia
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  • Omar L. Kantidze,

    Corresponding author
    1. Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia
    2. LIA 1066 French-Russian Joint Cancer Research Laboratory, France, Russia
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  • Sergey V. Razin

    1. Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia
    2. Department of Molecular Biology, Lomonosov Moscow State University, Moscow, Russia
    3. LIA 1066 French-Russian Joint Cancer Research Laboratory, France, Russia
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Abstract

Telomeric repeat binding factor 2 (TRF2) is a well-studied shelterin complex subunit that plays a major role in the protection of chomosome ends and the prevention of the telomere-associated DNA damage response. We show that heat shock induces the dissociation of TRF2 from telomeres in human primary and cancer cell cultures. TRF2 is not simply degraded in response to heat shock, but redistributed thoughout the nucleoplasm. This TRF2 depletion/redistribution does not initiate the DNA damage response at chomosome termini.

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