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81.
DNA放射损伤与p53 总被引:1,自引:0,他引:1
电离辐射等多种因素可以引起DNA损伤,表现为碱基改变、DNA双链断裂(DNA double-strand breaks,DSBs)和DNA单链断裂(Single-strand breaks,SSBs)等多种形式。DNA损伤后,细胞发生应答,即引起细胞周期阻滞和/或细胞程序性死亡,以减少损伤引起的染色体畸变和基因组不稳定。在细胞应答过程中,p53蛋白水平和活性均发生变化,介导细胞周期阻滞、程序性死亡,并直接参与DNA损伤修复过程。 相似文献
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Gai Liu Han Tian Yun-Qing Huang Jun Hu Yan-Xiao Ji Shao-Qing Li Yu-Qi Feng Lin Guo Ying-Guo Zhu 《The Journal of biological chemistry》2012,287(47):40051-40060
It has been suggested that the mitochondrial chimeric gene orfH79 is the cause for abortion of microspores in Honglian cytoplasmic male sterile rice, yet little is known regarding its mechanism of action. In this study, we used a mass spectrometry-based quantitative proteomics strategy to compare the mitochondrial proteome between the sterile line Yuetai A and its fertile near-isogenic line Yuetai B. We discovered a reduced quantity of specific proteins in mitochondrial complexes in Yuetai A compared with Yuetai B, indicating a defect in mitochondrial complex assembly in the sterile line. Western blotting showed that ORFH79 protein and ATP1 protein, an F1 sector component of complex V, are both associated with large protein complexes of similar size. Respiratory complex activity assays and transmission electron microscopy revealed functional and morphological defects in the mitochondria of Yuetai A when compared with Yuetai B. In addition, we identified one sex determination TASSELSEED2-like protein increased in Yuetai A, leading to the discovery of an aberrant variation of the jasmonic acid pathway during the development of microspores. 相似文献
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朱应葆 《中国生物化学与分子生物学报》1995,11(5):541-550
利用缺口修复(gaprepair)方法克隆啤酒酵母(S.cerevisiae)野生型RAD_(24)基因,并将其亚克隆到M13mp18和M13mp19,用双脱氧末端终止法对该基因的两条链均进行了序列测定。DNAStrider程序分析显示该基因编码268个氨基酸的蛋白质;基因缺失试验表明,该基因为细胞生存所必需。 相似文献
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Using resonance light scattering and UV/vis absorption spectroscopy to study the interaction between gliclazide and bovine serum albumin
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At different temperatures (298, 310 and 318 K), the interaction between gliclazide and bovine serum albumin (BSA) was investigated using fluorescence quenching spectroscopy, resonance light scattering spectroscopy and UV/vis absorption spectroscopy. The first method studied changes in the fluorescence of BSA on addition of gliclazide, and the latter two methods studied the spectral change in gliclazide while BSA was being added. The results indicated that the quenching mechanism between BSA and gliclazide was static. The binding constant (Ka), number of binding sites (n), thermodynamic parameters, binding forces and Hill's coefficient were calculated at three temperatures. Values for the binding constant obtained using resonance light scattering and UV/vis absorption spectroscopy were much greater than those obtained from fluorescence quenching spectroscopy, indicating that methods monitoring gliclazide were more accurate and reasonable. In addition, the results suggest that other residues are involved in the reaction and the mode ‘point to surface’ existed in the interaction between BSA and gliclazide. Copyright © 2015 John Wiley & Sons, Ltd. 相似文献
90.
ASPM and CITK regulate spindle orientation by affecting the dynamics of astral microtubules
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Marta Gai Federico T Bianchi Cristiana Vagnoni Fiammetta Vernì Silvia Bonaccorsi Selina Pasquero Gaia E Berto Francesco Sgrò Alessandra MA Chiotto Laura Annaratone Anna Sapino Anna Bergo Nicoletta Landsberger Jacqueline Bond Wieland B Huttner Ferdinando Di Cunto 《EMBO reports》2016,17(10):1396-1409
Correct orientation of cell division is considered an important factor for the achievement of normal brain size, as mutations in genes that affect this process are among the leading causes of microcephaly. Abnormal spindle orientation is associated with reduction of the neuronal progenitor symmetric divisions, premature cell cycle exit, and reduced neurogenesis. This mechanism has been involved in microcephaly resulting from mutation of ASPM, the most frequently affected gene in autosomal recessive human primary microcephaly (MCPH), but it is presently unknown how ASPM regulates spindle orientation. In this report, we show that ASPM may control spindle positioning by interacting with citron kinase (CITK), a protein whose loss is also responsible for severe microcephaly in mammals. We show that the absence of CITK leads to abnormal spindle orientation in mammals and insects. In mouse cortical development, this phenotype correlates with increased production of basal progenitors. ASPM is required to recruit CITK at the spindle, and CITK overexpression rescues ASPM phenotype. ASPM and CITK affect the organization of astral microtubules (MT), and low doses of MT‐stabilizing drug revert the spindle orientation phenotype produced by their knockdown. Finally, CITK regulates both astral‐MT nucleation and stability. Our results provide a functional link between two established microcephaly proteins. 相似文献