共查询到20条相似文献,搜索用时 15 毫秒
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Telomerase supports the proliferation of progenitor cells and tumor cells by adding telomere repeats to chromosome ends. The low abundance and restricted expression pattern of telomerase have limited our knowledge of this important enzyme. A new telomerase protein, TCAB1, sheds light on the pathway that governs telomerase holoenzyme assembly and function in vivo. TCAB1 is a component of active telomerase and is required for the telomerase holoenzyme to accumulate in Cajal bodies and to elongate telomeres. These findings provide important new insights into how telomerase functions in cancer and in stem cell biology. 相似文献
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Masashi Okabe Shigeru Saito Takeshi Saito Keizo Ito Shinzo Kimura Tadashi Niioka Masaaki Kurasaki 《Free radical biology & medicine》1998,24(9):1470-1476
Histochemical localization of superoxide anion (O2·−) scavenging activity in rat brain was visualized by the tissue-blotting technique. The activity was thought to mainly depend on Cu/Zn-SOD, because the localization of the activity was identical with the immunohistochemistry of Cu/Zn-SOD and the localization of its mRNA in the brain. Moreover, the activity was dramatically decreased after treatment of Cu (I) chelater. The activity was detected in pyramidal cells of the cortex, granular, and mitral cells of the olfactory bulbs, pyramidal cell layer CA1 to CA3, and dentate gyrus of hippocampus formation and granular cells of the cerebellum. Moreover, the activity was detected in the pontine nuclei of brain stem. Olfactory bulbs, hippocampus, and cerebellum were believed to be bestowed high brain functions, i.e., long-term potentiation and long-term depression. A part of the function was regulated by a retrograde neurotransmitter, nitric oxide (·NO). Our findings suggest that the SOD is colocalized with NO synthase in olfactory bulbs, hippocampus, and cerebellum, where ·NO plays the important roles. In contrast, low SOD activity was observed in the axonal neurofiber bundles, although the regions contain a lot of membrane lipids, which was thought to be peroxidized by O2·− and related radicals such as ·OH in the regions. From these findings, it was suggested that the SOD did not only play a role in protecting the neurons from endogenously formed O2·−, but also play a role in preservation of beneficial natures of ·NO in the brain. 相似文献
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Hae-Yun Jung Xin Wang Sohee Jun Jae-Il Park 《The Journal of biological chemistry》2013,288(10):7252-7262
Telomerase maintains the telomere, a specialized chromosomal end structure that is essential for genomic stability and cell immortalization. Telomerase is not active in most somatic cells, but its reactivation is one of the hallmarks of cancer. In this study, we found that dual-specificity tyrosine-(Y)-phosphorylation-regulated kinase 2 (Dyrk2) negatively regulates telomerase activity. Dyrk2 phosphorylates TERT protein, a catalytic subunit of telomerase. Phosphorylated TERT is then associated with the EDD-DDB1-VprBP E3 ligase complex for subsequent ubiquitin-mediated TERT protein degradation. During the cell cycle, Dyrk2 interacts with TERT at the G2/M phase and induces degradation. In contrast, depletion of endogenous Dyrk2 disrupts the cell cycle-dependent regulation of TERT and elicits the constitutive activation of telomerase. Similarly, a Dyrk2 nonsense mutation identified in breast cancer compromises ubiquitination-mediated TERT protein degradation. Our findings suggest the novel molecular mechanism of kinase-associated telomerase regulation. 相似文献
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The pleiotropy of telomerase against cell death 总被引:5,自引:0,他引:5
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Telomerase regulation and stem cell behaviour 总被引:24,自引:0,他引:24
Telomerase expression is restricted to a few cell types of the adult organism, most notably germ cells and stem/progenitor cells. Telomerase activity in germ cells is sufficient to prevent telomere shortening with age. Stem cells, however, do not have sufficient telomerase to prevent telomere shortening associated with continuous tissue renewal with increasing age. Indeed, telomerase levels in the adult organism are thought to be rate-limiting for longevity. This is supported by rare human syndromes caused by mutations in telomerase components, which are characterized by premature loss of tissue renewal and premature death. More recently, the role of telomerase and telomere length in stem cells is starting to be elucidated. 相似文献