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dc.contributor.authorChandra, J
dc.contributor.authorOzen, Mustafa
dc.contributor.authorPathak, S
dc.contributor.authorKumar, V
dc.contributor.authorMcConkey, DJ
dc.contributor.authorNewman, RA
dc.contributor.authorMultani, AS
dc.contributor.authorNarayan, S
dc.date.accessioned2021-03-05T12:05:01Z
dc.date.available2021-03-05T12:05:01Z
dc.date.issued2000
dc.identifier.citationMultani A., Ozen M., Narayan S., Kumar V., Chandra J., McConkey D., Newman R., Pathak S., "Caspase-dependent apoptosis induced by telomere cleavage and TRF2 loss", NEOPLASIA, cilt.2, ss.339-345, 2000
dc.identifier.issn1522-8002
dc.identifier.otherav_ab52874a-e5cc-47fb-a0a9-17dda407749b
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/114384
dc.identifier.urihttps://doi.org/10.1038/sj.neo.7900105
dc.description.abstractChromosomal abnormalities involving telomeric associations (TAs) often precede replicative senescence and abnormal chromosome configurations. We report here that telomere cleavage following exposure to pro-apoptotic agents is an early event in apoptosis, Exposure of human and murine cancer cells to a variety of pro-apoptotic stimuli (staurosporine, thapsigargin, anti-fas antibody, and cancer chemotherapeutic agents) resulted in telomere cleavage and aggregation, and finally their extrusion from the nuclei. Telomere loss was associated with arrest of cells in G(2)/M phase and preceded DNA fragmentation. Telomere erosion and subsequent large-scale chromatin cleavage were inhibited by overexpression of the anti-apoptotic protein, bcl-2, and two peptide caspase inhibitors (BACMK and zVADfmk), indicating that both events are regulated by caspase activation. The results demonstrate that telomere cleavage is an early chromatin alteration detected in various cancer cell lines leading to drug-induced apoptosis, and suggest that this event contributes to mitotic catastrophe and induction of cell death. Results also suggest that the decrease of telomeric-repeat binding factor 2 (TRF2) may be the earliest event in the ara-C-induced telomere shortening, induction of endoreduplication and chromosomal fragmentation leading to cell death.
dc.language.isoeng
dc.subjectOnkoloji
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectİç Hastalıkları
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectONKOLOJİ
dc.titleCaspase-dependent apoptosis induced by telomere cleavage and TRF2 loss
dc.typeMakale
dc.relation.journalNEOPLASIA
dc.contributor.department, ,
dc.identifier.volume2
dc.identifier.issue4
dc.identifier.startpage339
dc.identifier.endpage345
dc.contributor.firstauthorID58455


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