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131.
抑制O~6-甲基鸟嘌呤-DNA甲基转移酶活性与肿瘤细胞对亚硝脲药物敏感性关系的研究 总被引:1,自引:0,他引:1
80%以上的肿瘤细胞为O~6-甲基鸟嘌吟-DNA甲基转移酶(O~6-MT)活性较高的Mer~+型,能够修复亚硝脲药物(NU)造成的DNA烷化损伤,对NU不敏感。本实验证明,用0.75,0.50和0.25mmol/L甲基亚硝脲(MNU)分别处理Mer~+型的HeLaS3,SMMC-7721和表现Mer~-型特征的Cc801,均能明显降低细胞中O~6-MT活性,从而显著提高了三种细胞对嘧啶亚硝脲和双氯乙亚硝脲的敏感性,提示降低O~6-MT活性是使用NU对Mer~+型肿瘤进行有效治疗的前提。 相似文献
132.
据我们在北京和内蒙古等地多年研究表明,黄芪的植食性种子小蜂包括广肩小蜂科Bruchophagus属5种和金小蜂科Habrocytus属1种,为多种混合群体。我们通过大量标本的形态比较以及交配行为的观察,结合其生物学特性研究以及应用扫描电镜对其并胸腹节花纹的超微结构观察,鉴定出黄芪种子里有5种广肩种子小蜂,即黄芪种子小蜂Bruchophagus huonchi Liao et Fan及本文的4新种。 相似文献
133.
在自行建立的人工海洋小生境中,采用示踪法综合地研究~(137)Cs、~(134)Cs在人工小生境中的行为。结果表明,~(137)Cs和~(134)Cs具有共同的生理生态行为,并表现出相似的规律、沉积物对~(137)Cs、~(134)Cs的吸附能力甚低,~(137)Cs、~(134)Cs在海洋动物体内趋于全身性的分布。各主要生化物质均能检出~(137)Cs、~(134)Cs。排泄实验后,海洋动物的胃肠、肝(消化腺)~(137)Cs、~(134)Cs损失显著。沉积物表现为解吸-重吸附的过程。 相似文献
134.
Caveolin, a protein component of caveolae membrane coats. 总被引:141,自引:0,他引:141
Caveolae have been implicated in the transcytosis of macromolecules across endothelial cells and in the receptor-mediated uptake of 5-methyltetrahydrofolate. Structural studies indicate that caveolae are decorated on their cytoplasmic surface by a unique array of filaments or strands that form striated coatings. To understand how these nonclathrin-coated pits function, we performed structural analysis of the striated coat and searched for the molecular component(s) of the coat material. The coat cannot be removed by washing with high salt; however, exposure of membranes to cholesterol-binding drugs caused invaginated caveolae to flatten and the striated coat to disassemble. Antibodies directed against a 22 kd substrate for v-src tyrosine kinase in virus-transformed chick embryo fibroblasts decorated the filaments, suggesting that this molecule is a component of the coat. We have named the molecule caveolin. Caveolae represent a third type of coated membrane specialization that is involved in molecular transport. 相似文献
135.
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137.
Uwe G. Goehlert N. M. K. Ng Ying Kin Leonhard S. Wolfe 《Journal of neurochemistry》1981,36(3):1192-1201
Abstract: Microvessels, predominantly capillaries, were isolated from rat cerebrum by a modification of published procedures. The morphology and purity of the preparations were monitored by light and electron microscopy and by enrichment in alkaline phosphatase, γ-glutamyl transpeptidase, and prostacyclin synthetase. A reversed-phase high-pressure liquid chromatographic method was used in the purification of prostaglandins after extraction from aqueous incubation solutions. Prostacyclin synthesis in brain is localized in cerebral blood vessels and capillaries. The endogenous biosynthetic capacity of the isolated cerebral capillary fractions for prostacyclin, measured as its chemically stable breakdown product, 6-keto-prostaglandin F1α , was 11 ng/mg protein/10 min. Choroid plexus and intact surface vessels synthesized 6-keto-prostaglandin F1α at 37 and 35 ng/mg protein/10 min, respectively. The prostacyclin-synthesizing enzyme of the cerebral capillaries also converted the exogenously added prostaglandin endoperoxides to 6-keto-prostaglandin F1α . Comparison of the synthesis of prostaglandins 6-keto-F1α , E2 , and F2α showed that 6-keto-prostaglandin F1α was the major prostaglandin formed in the microvessels, in the larger surface vessels, and in the choroid plexus. Prostaglandin D2 was not detected. Prostacyclin synthesis by the cerebral vasculature is similar to that in other blood vessels and cultured human endothelial cells. Possible physiological roles of prostacyclin in the cerebral microvasculature are discussed with special regard to the autoregulation of cerebral blood flow. 相似文献
138.
Repeated Biogel P6 chromatography of the urine from a patient with fucosidosis yielded several fractions containing fucosyloligosaccharides and glycopeptides. Two of these were shown by 1H nuclear magnetic resonance (1H-n.m.r.) spectroscopy and permethylation analysis to have the following structures respectively: (I) αfuc (1→3) [βgal (1→4)] βglcNAc (1→2) αman () βman (1→4) glcNAc and (II) αfuc (1→3) [βgal (1→4)] βglcNAc (1→2) αman () βman (1→4) βglcNAc (1→4) [αfuc ()] βglcNAc-Asn. 相似文献
139.
ZAKβ antagonizes and ameliorates the cardiac hypertrophic and apoptotic effects induced by ZAKα 下载免费PDF全文
Chien‐Yao Fu Wei‐Wen Kuo Tsung‐Jung Ho Su‐Ying Wen Ling‐Chun Lin Yan‐Shen Tseng Hui‐Chuan Hung Vijaya Padma Viswanadha Chih‐Yang Huang 《Cell biochemistry and function》2016,34(8):606-612
ZAK (sterile alpha motif and leucine zipper containing kinase AZK), a serine/threonine kinase with multiple biochemical functions, has been associated with various cell processes, including cell proliferation, cell differentiation, and cardiac hypertrophy. In our previous reports, we found that the activation of ZAKα signaling was critical for cardiac hypertrophy. In this study, we show that the expression of ZAKα activated apoptosis through both a FAS‐dependent pathway and a mitochondria‐dependent pathway by subsequently inducing caspase‐3. ZAKβ, an isoform of ZAKα, is dramatically expressed during cardiac hypertrophy and apoptosis. The interaction between ZAKα and ZAKβ was demonstrated here using immunoprecipitation. The results show that ZAKβ has the ability to diminish the expression level of ZAKα. These findings reveal an inherent regulatory role of ZAKβ to antagonize ZAKα and to subsequently downregulate the cardiac hypertrophy and apoptosis induced by ZAKα. 相似文献
140.