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Telomere attrition and dysfunction: a potential trigger of the progeroid phenotype in nijmegen breakage syndrome

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F20%3A10412829" target="_blank" >RIV/00216208:11130/20:10412829 - isvavai.cz</a>

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Qd90OGisq9" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Qd90OGisq9</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.18632/aging.103453" target="_blank" >10.18632/aging.103453</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Telomere attrition and dysfunction: a potential trigger of the progeroid phenotype in nijmegen breakage syndrome

  • Original language description

    Background: Nibrin, as part of the NBN/MRE11/RAD50 complex, is mutated in Nijmegen breakage syndrome (NBS), which leads to impaired DNA damage response and lymphoid malignancy. Results: Telomere length (TL) was markedly reduced in homozygous patients (and comparably so in all chromosomes) by similar to 40% (qPCR) and was slightly reduced in NBS heterozygotes older than 30 years (similar to 25% in qPCR), in accordance with the respective cancer rates. Humanized cancer-free NBS mice had normal TL. Telomere elongation was inducible by telomerase and/or alternative telomere lengthening but was associated with abnormal expression of telomeric genes involved in aging and/or cell growth. Lymphoblastoid cells from NBS patients with long survival times (&gt;12 years) displayed the shortest telomeres and low caspase 7 activity. Conclusions: NBS is a secondary telomeropathy. The two-edged sword of telomere attrition enhances the cancer-prone situation in NBS but can also lead to a relatively stable cellular phenotype in tumor survivors. Results suggest a modular model for progeroid syndromes with abnormal expression of telomeric genes as a molecular basis. Methods: We studied TL and function in 38 homozygous individuals, 27 heterozygotes, one homozygous fetus, six NBS lymphoblastoid cell lines, and humanized NBS mice, all with the same founder NBN mutation: c.657_661del5.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10600 - Biological sciences

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Aging

  • ISSN

    1945-4589

  • e-ISSN

  • Volume of the periodical

    12

  • Issue of the periodical within the volume

    12

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    34

  • Pages from-to

    12342-12375

  • UT code for WoS article

    000548154300016

  • EID of the result in the Scopus database

    2-s2.0-85087363080