WordNet
- the time when something ends; "it was the death of all his plans"; "a dying of old hopes" (同)dying, demise
- the time at which life ends; continuing until dead; "she stayed until his death"; "a struggle to the last" (同)last
- the absence of life or state of being dead; "he seemed more content in death than he had ever been in life"
- the permanent end of all life functions in an organism or part of an organism; "the animal died a painful death"
- the act of killing; "he had two deaths on his conscience"
- the event of dying or departure from life; "her death came as a terrible shock"; "upon your decease the capital will pass to your grandchildren" (同)decease, expiry
- the personification of death; "Death walked the streets of the plague-bound city"
PrepTutorEJDIC
- 〈U〉〈C〉『死』,死亡;死に方,死にざま / 〈U〉死んだ[ような]状体 / 《the~》(…の)絶滅,破滅《+『of』+『名』》 / 《the~》(…の)死の原因,命取り《+『of』+『名』》 / 《通例『D-』》死神(手に鎌(かマ)を持った黒装束の骸骨(がいこつ)で表される)
UpToDate Contents
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English Journal
- βTrCP-mediated ubiquitylation regulates protein stability of Mis18β in a cell cycle-dependent manner.
- Kim IS1, Lee M1, Park JH2, Jeon R3, Baek SH1, Kim KI4.Author information 1Department of Biological Sciences, Creative Research Initiative Center for Chromatin Dynamics, Seoul National University, Seoul 151-742, South Korea.2Department of Biological Sciences, Sookmyung Women's University, Seoul 140-742, South Korea.3Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140-742, South Korea.4Department of Biological Sciences, Sookmyung Women's University, Seoul 140-742, South Korea. Electronic address: kikim@sookmyung.ac.kr.AbstractUbiquitin E3 ligases including SCF complex are key regulators of cell cycle. Here, we show that Mis18β, a component of Mis18 complex governing CENP-A localization, is a new substrate of βTrCP-containing SCF complex. βTrCP interacted with Mis18β exclusively during interphase but not during mitosis and mediated proteasomal degradation of Mis18β leading to the inactivation of Mis18 complex during interphase. In addition, uncontrolled stabilization of Mis18β caused cell death. Together, we propose that βTrCP-mediated regulation of Mis18β stability is a mechanism to restrict centromere function of Mis18 complex from late mitosis to early G1 phase.
- Biochemical and biophysical research communications.Biochem Biophys Res Commun.2014 Jan 3;443(1):62-7. doi: 10.1016/j.bbrc.2013.11.058. Epub 2013 Nov 21.
- Ubiquitin E3 ligases including SCF complex are key regulators of cell cycle. Here, we show that Mis18β, a component of Mis18 complex governing CENP-A localization, is a new substrate of βTrCP-containing SCF complex. βTrCP interacted with Mis18β exclusively during interphase but not during mitosi
- PMID 24269809
- Micronucleus frequencies and clonogenic cell survival in TK6 cells exposed to changing dose rates under controlled temperature conditions.
- Brehwens K, Bajinskis A, Haghdoost S, Wojcik A.AbstractAbstract Purpose: In most exposure scenarios the dose rate of exposure is not constant. Despite this, very little information exists on the possible biological effects of exposing cells to radiation under the conditions of a changing dose rate. The current study highlights interesting effects following exposure under these conditions. Materials and methods: We constructed a new exposure facility that allows exposing cells inside an incubator and used it to irradiate human lymphoblastoid TK6 cells both after a moderate (0.48 Gy) and a high (1.1 Gy) dose, where the change in dose rate was, respectively, ≈ 17-fold change (2.2 - 37 mGy/min) and ≈ 39-fold (2.7 - 106 mGy/min). Clonogenic survival and micronuclei (MN) induction were the chosen endpoints. Results: The obtained results confirm the outcome of our first study that TK6 cells exposed to a decreasing dose rate express more MN than cells exposed to an increasing or constant dose rate. The effect was not seen after the moderate dose of 0.48 Gy or detectable at the level of clonogenic cell survival. Conclusions: We speculate that the high level of MN is probably related to a delayed elimination of damaged cells by interphase death, as opposed to mechanisms relating to DNA damage and repair.
- International journal of radiation biology.Int J Radiat Biol.2013 Dec 18. [Epub ahead of print]
- Abstract Purpose: In most exposure scenarios the dose rate of exposure is not constant. Despite this, very little information exists on the possible biological effects of exposing cells to radiation under the conditions of a changing dose rate. The current study highlights interesting effects follow
- PMID 24350915
- Dissimilar effects of β-lapachone- and hydroxyurea-induced DNA replication stress in root meristem cells of Allium cepa.
- Zabka A, Trzaskoma P, Maszewski J.Author information Department of Cytophysiology, Faculty of Biology and Environmental Protection, University of Łódź, Pomorska 141/143, 90-236 Łódź, Poland. Electronic address: zabkka@poczta.onet.pl.AbstractTwo anticancer drugs, β-lapachone (β-lap, a naphthoquinone) and hydroxyurea (HU, an inhibitor of ribonucleotide reductase), differently affect nuclear morphology and cell cycle control mechanisms in root meristem cells of Allium cepa. The 18 h treatment with 100 μM β-lap results in a lowered number of M-phase cells, increased occurrence of mitotic abnormalities, including over-condensation of chromosomes, their enhanced stickiness, formation of anaphase bridges, micronucleation and reduced mitotic spindles. Following prolonged incubations using high doses of β-lap, cell nuclei reveal dark-red fluorescence evenly distributed in chromatin surrounding the unstained regions of nucleoli. Both drugs generate H2O2 and induce DNA double strand breaks, which is correlated with γ-phoshorylation of H2AX histones. However, the extent of H2AX phosphorylation (including the frequency of γ-H2AX foci and the relative number cells creating phospho-H2AX domains) is considerably reduced in root meristem cells treated jointly with the β-lap/HU mixture. Furthermore, various effects of caffeine (an inhibitor of ATM/ATR cell cycle checkpoint kinases) on β-lap- and HU-induced γ-phoshorylation of H2AX histones and the protective activity of HU against β-lap suggest that their genotoxic activities are largely dissimilar. β-Lap treatment results in the induction of apoptosis-like programmed cell death, while HU treatment leads to cell adaptation to replication stress and promotion of abnormal nuclear divisions with biphasic interphase/mitotic states of chromatin condensation.
- Plant physiology and biochemistry : PPB / Société française de physiologie végétale.Plant Physiol Biochem.2013 Dec;73:282-93. doi: 10.1016/j.plaphy.2013.10.001. Epub 2013 Oct 11.
- Two anticancer drugs, β-lapachone (β-lap, a naphthoquinone) and hydroxyurea (HU, an inhibitor of ribonucleotide reductase), differently affect nuclear morphology and cell cycle control mechanisms in root meristem cells of Allium cepa. The 18 h treatment with 100 μM β-lap results in a lowered n
- PMID 24184448
Japanese Journal
- 子宮内胎児死亡の原因検索に頬粘膜細胞による間期核FISH法が有用であった1症例
- High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis
- Exploration of 'Over Kill Effect' of High-LET Ar-and Fe-ions by Evaluating the Fraction of Non-hit Cell and Interphase Death
Related Links
- "interphase death" への豊富な翻訳例文 – 和英辞書と日本語翻訳サーチエンジン ... 辞書 英語-日本語
- 1. Int J Radiat Biol Relat Stud Phys Chem Med. 1988 Jan;53(1):65-75. Radiation-induced interphase death of rat thymocytes is internally programmed (apoptosis). Yamada T(1), Ohyama H. Author information: (1)Division of ...
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