Zobrazeno 1 - 10 of 208 pro vyhledávání: '"Marcu, K."'
2
Regulated transcription of human matrix metalloproteinase 13 (MMP13) and interleukin-1β (IL1B) genes in chondrocytes depends on methylation of specific proximal promoter CpG sites
Autor: Hashimoto, K., Otero, M., Imagawa, K., De Andrés González, Mª Carmen, Coico, J. M., Roach, H. I., Oreffo, R. O. C., Marcu, K. B., Goldring, M. B.
Publikováno v: RUNA. Repositorio da Consellería de Sanidade e Sergas
Servizo Galego de Saúde (SERGAS)
The role of DNA methylation in the regulation of catabolic genes such as MMP13 and IL1B, which have sparse CpG islands, is poorly understood in the context of musculoskeletal diseases. We report that demethylation of specific CpG sites at -110 bp and
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::270aafa864200c7e5520bb5513be0f00
http://hdl.handle.net/20.500.11940/3542
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7
Chronic NF-kappaB activation delays RasV12-induced premature senescence of human fibroblasts by suppressing the DNA damage checkpoint response
Autor: Batsi, C., Markopoulou, S., Vartholomatos, G., Georgiou, I., Kanavaros, P., Gorgoulis, V. G., Marcu, K. B., Kolettas, E.
Normal cells divide for a limited number of generations, after which they enter a state of irreversible growth arrest termed replicative senescence. While replicative senescence is due to telomere erosion, normal human fibroblasts can undergo stress-
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_____10561::48e40c5e925439aa637771414d11af51
http://olympias.lib.uoi.gr/jspui/handle/123456789/23125
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8
Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27(Kip1)-dependent G1/S cell cycle arrest in conjunction with NF-kappaB activation
Autor: Batsi, C., Markopoulou, S., Kontargiris, E., Charalambous, C., Thomas, C., Christoforidis, S., Kanavaros, P., Constantinou, A. I., Marcu, K. B., Kolettas, E.
2-Methoxyestradiol (2-ME2) induces leukemia cells to undergo apoptosis in association with Bcl-2 inactivation but the mechanisms whereby Bcl-2 contributes to protection against programmed cell death in this context remain unclear. Here we showed that
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_____10561::910d65207ed918752b5803f7d2216cff
http://olympias.lib.uoi.gr/jspui/handle/123456789/23528
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Plný text Recenzováno Digitální knihovna AV ČR
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