Lamin B receptor (LBR) is involved in the induction of cellular senescence in human cells
| Autor: | Yuki Takauji, Dai Ayusawa, Michihiko Fujii, Atsuki En, Kensuke Miki, Keisuke Maki, Rumi Arai |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
DNA Replication Aging Somatic cell Nuclear Envelope Receptors Cytoplasmic and Nuclear Lamin B receptor HeLa 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Heterochromatin medicine Humans Heterochromatin organization Fibroblast Cellular Senescence biology Lamin Type B Chemistry biology.organism_classification Cell biology Chromatin 030104 developmental biology medicine.anatomical_structure Bromodeoxyuridine Gene Knockdown Techniques Thymidine 030217 neurology & neurosurgery Function (biology) Developmental Biology DNA Damage HeLa Cells |
| Zdroj: | Mechanisms of ageing and development. 178 |
| ISSN: | 1872-6216 |
| Popis: | Cellular senescence is a phenomenon of irreversible growth arrest in mammalian somatic cells in culture. Various stresses induce cellular senescence and indeed, we have found that excess thymidine effectively induces cellular senescence in human cells. Further, many reports indicate the implication of chromatin proteins in cellular senescence. Here we analysed the role of lamin B receptor (LBR), a nuclear envelope protein that regulates heterochromatin organization, in cellular senescence induced by excess thymidine. We then found that the LBR protein was down-regulated and showed aberrant localization in cells upon induction of cellular senescence by excess thymidine. Additionally, we also found that knock-down of LBR facilitated the induction of cellular senescence by excess thymidine in cancerous HeLa cells, and importantly, it induced cellular senescence in normal human diploid fibroblast TIG-7 cells. These results suggested that decreased LBR function is involved in the induction of cellular senescence in human cells. |
| Databáze: | OpenAIRE |
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