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51.
52.
Oncogenic activation of the human trk proto-oncogene by recombination with the ribosomal large subunit protein L7a. 总被引:10,自引:0,他引:10
The trk-2h oncogene, isolated from the human breast carcinoma cell line MDA-MB 231 by genomic DNA-transfection into NIH3T3 cells, consists of the trk proto-oncogene receptor kinase domain fused to a N-terminal 41 amino acid activating sequence (Kozma, S.C., Redmond, S.M.S., Xiao-Chang, F., Saurer, S.M., Groner, B. and Hynes, N.E. (1988) EMBO J., 7, 147-154). Antibodies raised against a bacterially produced beta gal-trk receptor kinase fusion protein recognized a 44 kd phosphoprotein phosphorylated on serine, threonine and tyrosine in extracts of trk-2h transformed NIH3T3 cells. In vitro, in the presence of Mn2+/gamma ATP, this protein became phosphorylated extensively on tyrosine. Cells transformed by trk-2h did not, however, show an elevation in total phosphotyrosine. We have cloned and sequenced the cDNA encoding the amino terminal activating sequences of trk-2h (Kozma et al., 1988). The encoded protein has a high basic amino acid content and the gene is expressed as an abundant 1.2 kb mRNA in human, rat and mouse cells. Antipeptide antibodies raised against a C-terminal peptide recognized specifically a 30 kd protein on Western blots of human, rat and mouse cell extracts. Immunofluorescence revealed, in addition to granular cytoplasmic fluorescence, intense nucleolar staining. The high basic amino acid content and nucleolar staining prompted us to investigate whether the 30 kd protein could be a ribosomal protein. Western immunoblotting analysis of 2D-electrophoretically resolved ribosomal proteins indicated that the 30 kd protein is the ribosomal large subunit protein L7a.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
53.
对长春和北京地区连续12年(1976年冬至1988年春)引起小儿肺炎的3、7型腺病毒102株标本,进行了限制性内切酶核酸电泳图谱分析。56株7型腺病毒经BamHⅠ、BclⅠ、BglⅠ、XbaⅠ、SmaⅠ、HindⅢ分析后,表现为两个基因组型——Ad7 b和Ad7 d。46株3型腺病毒被Bg1 Ⅱ、BamHⅠ酶解后,表现为 3个基因组型——Ad 3Ⅰ、Ad 3Ⅱ、Ad 3Ⅲ。各基因组型的分布情况是:56株7型腺病毒中,43株为Ad 7 b(76.8%),流行于1976年冬至1986年春;13株是Ad 7 d(23.2%),出现于1982年,与Ad 7 b共同流行;1986年~1988年分析的5株病毒都是Ad 7d。43株3型腺病毒中,Ad3Ⅰ42株(91.0%),分布于12年中;Ad 3Ⅱ、Ad 3Ⅲ各2株,散在分布。此结果表明,国内这12年中引起小儿肺炎的3型腺病毒至少有3个基因组型,7型腺病毒至少有两个基因组型。Ad3Ⅰ和Ad7 b是流行优势基因组型。但自80年代初开始出现Ad7 d以来,有逐年增多的趋势,最近两年的标本又都是Ad7 d,很可能它将取代Ad7 b而成为流行的优势基因组型. 相似文献
54.
在肉色诺卡氏菌C-212株Nocardia carnea C-212中筛选到一种Ⅱ型限制性核酸内切酶NcrⅠ,经与BglⅡ的λDNA降解物的酶谱比较,以及酶识别特异性和切割位点的检测,证明了NcrⅠ是已知的限制酶BglⅡ的同切限制酶,而且其切割位点也与BglⅡ相同,其为: 相似文献
55.
黄皮种子发育过程中脱水敏感性与细胞膜透性的关系 总被引:3,自引:0,他引:3
黄皮(Clausena lansium (Lour.) Skeels)胚轴与完整种子的发育模式以及发育中电解质渗漏率变化有些不同. 种子生理成熟前、后的胚轴对脱水的反应也不同,前者经轻微脱水可提高萌发率和活力指数,后者不耐任何程度的脱水.活力指数的急剧下降伴随着电解质渗漏率的迅速上升.实验表明,黄皮种子在发育过程中没有形成耐脱水性. 细胞膜透性变化可反映脱水对种子的伤害程度 相似文献
56.
The localization of the ai adrenoceptors (1-AR) in the heart tissues from rat and human and in the cultured heart cells from neonatal rats was studied by indirect immunofluorescence and postembedding electronmicroscopical immuno-gold technique. With antipeptide antibodies directed against the second extracellular loop of the human 1-AR (AS sequence 192–218), this receptor was found to be localized along the sarcolemma in both human and rat hearts. Similar localization sites were detected in cultivated rat neonatal cardiomyocytes. Beside the localization in cardiomyocytes, 1-AR were identified in endothelial cells of capillaries and smooth muscle cells of coronary vessels, in neuronal endings, in mast cells of cultivated heart cells but not, or in less amount in fibroblasts. Interestingly, in the right atrium of rat heart the localization of 1-AR was found to be near or on atrial natriuretic factor (ANF) granules, providing the basis for the -adrenergic influence on ANF release. The immunocytochemical studies further confirm and complete the findings known by using autoradiographic binding studies with specific ligands. 相似文献
57.
Zhao Rongrui Wang Wenze Wu Bowei Hoebeke Johan Hjalmarson Åke Fu Michael L. X. 《Molecular and cellular biochemistry》1996,163(1):185-193
The effects of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic receptor on transmembrane potentials and currents in guinea pig single ventricular cells were analyzed using whole-cell patch clamp technique. These effects were compared with those of the muscarinic receptor agonists carbachol and acetylcholine. The antibodies shortened the action potential duration in a dose-dependent manner. By using a ramp or step rectangular pulse protocol, it was found that the antibodies increased the outward K+ current and decreased the inward basal I Ca significantly. The reversal potential of both carbachol-and antibody-induced extra currents were close to –80 mV, being in proximity to the calculated Ek of –90 mV. A -adrenergic receptor agonist, isoprenaline, prolonged the action potential and increased the overshoot which could be inhibited by both antibody and carbachol. Isoprenaline increased inward Ica and outward Ik simultaneously. Both antibody and carbachol could significantly reduce the isoprenaline-stimulated ICa but not the isoprenaline-stimulated Ik. The antibody- or carbachol-induced outward K+ current and the depressant effects of antibody and carbachol on isoprenaline-stimulated Ica were partially antagonized by atropine. These results suggest that the anti-M2 muscarinic receptor antibodies display a stimulatory activity similar to muscarinic receptor agonist on the receptor-mediated electrophysiological events. 相似文献
58.
中国沿海代表性河口地区鳗苗群体形态特征的比较研究 总被引:2,自引:0,他引:2
本文报道了1992—1994年连续3年采自海南至辽宁(包括台湾)沿海7个代表性河口地区鳗苗群体的主要形态特征比较研究结果。4项计数性状和3项度量性状,差异系数分析结果未达到亚种差异水平;判别函数显示,大多数群体间存在显著差异,这种差异应源于遗传变异。各年差异变化无规律,可能与鳗苗漂游分布的随机性有关。 相似文献
59.
Ronald W. Wilen Ping Fu Albert J. Robertson Suzanne R. Abrams Nicholas H. Low Lawrence V. Gusta 《Planta》1996,200(1):138-143
The application of abscisic acid (ABA), either as a racemic mixture or as optically resolved isomers, increases freezing tolerance in a bromegrass (Bromus inermis Leyss) cell culture and induces the accumulation of several heat-stable proteins. Two stereoisomers of an ABA analog, 23 dihydroacetylenic abscisyl alcohol (DHA), were used to study the role of ABA-induced processes in the acquisition of freezing tolerance in these cells. Freezing tolerance was unchanged in the presence of (–) DHA (LT50 -9°C), and no increase in heat-stable protein accumulation was detected; however, the (+) enantiomer increased the freezing tolerance (LT50 -13°C) and induced the accumulation of these polypeptides. All three forms of ABA increased freezing tolerance in the bromegrass cells, although (–) ABA was less effective than either (+) or (±) ABA when added at equal concentrations. Cells pretreated with 20 or 50 M (–) DHA displayed lower levels of freezing tolerance following the addition of 2.5, 7.5 or 25 M (±) ABA. Full freezing tolerance could be restored by increasing the concentration of (±) ABA to > 25 M. Pretreatment of cells with (–) DHA (20 or 50 M) had no effect on freezing tolerance when 25 M (+) ABA was added. The induction of freezing tolerance by 25 M (–) ABA was completely inhibited by the presence of 20 M (–) DHA. The accumulation of ABA-responsive heat-stable proteins was inhibited by pretreatment with 20 M (–) DHA in cells treated with 2.5 or 7.5M (+) ABA, and in cells treated with 25 M (–) ABA. The accumulation of these polypeptides was restored when (±) or (+) ABA was added at a concentration of 25 M. The analysis of proteins which cross-reacted with a dehydrin antibody revealed a similar inhibitory pattern as seen with the other ABA-responsive proteins. The effects of the various isomers of ABA and DHA on cell osmolarity and sucrose uptake was also investigated. In both cases, (±) and (+) ABA had pronounced effects on the parameters measured, whereas (–) ABA treated cells gave substantially different results. In both sucrose uptake and cell osmolarity, DHA had no significant effect on the results obtained following (±) or (+) ABA treatment. Maximum freezing tolerance was only observed in cells when both heat-stable protein accumulation and sucrose uptake were observed.Abbreviations ABA
abscisic acid
- DHA
2,3 dihydroacetylenicabscisyl alcohols
- DMSO
dimethyl sulfoxide
- LT50
temperature at which 50% of cells are killed
The authors would like to acknowledge the technical assistance of Angela Bollman, Bruce Ewan and Angela Shaw. This work was supported by grants from the Natural Science and Engineering Research Council of Canada to L.V.G. and N.H.L., and a grant from the University of Saskatchewan to R.W.W. 相似文献
60.
Lack of X inactivation associated with maternal X isodisomy: evidence for a counting mechanism prior to X inactivation during human embryogenesis. 总被引:4,自引:2,他引:2
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