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Consequences of Lamin B1 and Lamin B Receptor Downregulation in Senescence

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F18%3A00492528" target="_blank" >RIV/68081707:_____/18:00492528 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.3390/cells7020011" target="_blank" >http://dx.doi.org/10.3390/cells7020011</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/cells7020011" target="_blank" >10.3390/cells7020011</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Consequences of Lamin B1 and Lamin B Receptor Downregulation in Senescence

  • Original language description

    Anchoring of heterochromatin to the nuclear envelope appears to be an important process ensuring the spatial organization of the chromatin structure and genome function in eukaryotic nuclei. Proteins of the inner nuclear membrane (INM) mediating these interactions are able to recognize lamina-associated heterochromatin domains (termed LAD) and simultaneously bind either lamin A/C or lamin B1. One of these proteins is the lamin B receptor (LBR) that binds lamin B1 and tethers heterochromatin to the INM in embryonic and undifferentiated cells. It is replaced by lamin A/C with specific lamin A/C binding proteins at the beginning of cell differentiation and in differentiated cells. Our functional experiments in cancer cell lines show that heterochromatin in cancer cells is tethered to the INM by LBR, which is downregulated together with lamin B1 at the onset of cell transition to senescence. The downregulation of these proteins in senescent cells leads to the detachment of centromeric repetitive sequences from INM, their relocation to the nucleoplasm, and distension. In cells, the expression of LBR and LB1 is highly coordinated as evidenced by the reduction of both proteins in LBR shRNA lines. The loss of the constitutive heterochromatin structure containing LADs results in changes in chromatin architecture and genome function and can be the reason for the permanent loss of cell proliferation in senescence.

  • 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

    10601 - Cell biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Cells

  • ISSN

    2073-4409

  • e-ISSN

  • Volume of the periodical

    7

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    9

  • Pages from-to

  • UT code for WoS article

    000427516700002

  • EID of the result in the Scopus database