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- Espada, J, et al.
(författare)
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Nuclear envelope defects cause stem cell dysfunction in premature-aging mice
- 2008
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Ingår i: The Journal of cell biology. - : Rockefeller University Press. - 1540-8140 .- 0021-9525. ; 181:1, s. 27-35
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Tidskriftsartikel (refereegranskat)abstract
- Nuclear lamina alterations occur in physiological aging and in premature aging syndromes. Because aging is also associated with abnormal stem cell homeostasis, we hypothesize that nuclear envelope alterations could have an important impact on stem cell compartments. To evaluate this hypothesis, we examined the number and functional competence of stem cells in Zmpste24-null progeroid mice, which exhibit nuclear lamina defects. We show that Zmpste24 deficiency causes an alteration in the number and proliferative capacity of epidermal stem cells. These changes are associated with an aberrant nuclear architecture of bulge cells and an increase in apoptosis of their supporting cells in the hair bulb region. These alterations are rescued in Zmpste24−/−Lmna+/− mutant mice, which do not manifest progeroid symptoms. We also report that molecular signaling pathways implicated in the regulation of stem cell behavior, such as Wnt and microphthalmia transcription factor, are altered in Zmpste24−/− mice. These findings establish a link between age-related nuclear envelope defects and stem cell dysfunction.
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| 2. |
- Freije, JP, et al.
(författare)
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Localization of the human cystatin D gene (CST5) to chromosome 20p11.21 by in situ hybridization
- 1993
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Ingår i: Cytogenetics and Cell Genetics. - : S. Karger AG. - 0301-0171. ; 62:1, s. 29-31
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Tidskriftsartikel (refereegranskat)abstract
- The gene coding for cystatin D (CST5), a cysteine proteinase inhibitor, was mapped by fluorescent in situ hybridization to human chromosome 20p11.21. This assignment, together with previous data on mapping of members of the cystatin gene family, indicates that cystatin family II genes are all clustered on the short arm of chromosome 20, whereas cystatin family I and III genes are located on the long arm of chromosome 3.
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| 3. |
- Gomez, R, et al.
(författare)
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Dynamic localization of SMC5/6 complex proteins during mammalian meiosis and mitosis suggests functions in distinct chromosome processes
- 2013
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Ingår i: Journal of cell science. - : The Company of Biologists. - 1477-9137 .- 0021-9533. ; 126:18Pt 18, s. 4239-4252
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Tidskriftsartikel (refereegranskat)abstract
- Four members of the structural maintenance of chromosome (SMC) protein family have essential functions in chromosome condensation (SMC2/4) and sister-chromatid cohesion (SMC1/3). The SMC5/6 complex has been implicated in chromosome replication, DNA repair, and chromosome segregation in somatic cells, but its possible functions during mammalian meiosis are unknown. Here, we find that in mouse spermatocytes SMC5 and SMC6 are located at the central region of the synaptonemal complex from zygotene until diplotene. During late diplotene both proteins load to the chromocenters, where they colocalize with DNA Topoisomerase IIα, and then accumulate at the inner domain of the centromeres during the first and second meiotic divisions. Interestingly, SMC6 and DNA Topoisomerase IIα colocalize at stretched strands that join kinetochores during the metaphase II to anaphase II transition, and are both observed on stretched lagging chromosomes at anaphase II following Etoposide treatment. During mitosis SMC6 and DNA Topoisomerase IIα colocalize at the centromeres and chromatid axes. Our results are consistent with the participation of SMC5 and SMC6 in homologous chromosome synapsis during prophase I, chromosome and centromere structure during meiosis I and mitosis, and, with DNA Topoisomerase IIα, in regulating centromere cohesion during meiosis II.
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