自由基与软骨基质胶原蛋白类型改变

本文利用ＳＤＳ－聚丙烯酰胺凝胶电泳方法,定量研究了体外培养的软骨细胞和软骨组织基质中Ⅱ型胶原蛋白的含量。结果表明氧自由基（·Ｏ－２和·ＯＨ）和具有自由基性质的物质（黄腐酸,镰刀菌毒素）可使软骨细胞合成,分泌异常的非Ⅱ型的胶原蛋白,同时,硒化合物可明显地抑制此种效应。     

钙／钙调素依赖性蛋白激酶对17．7kD和6kD胰腺蛋白的磷酸化

本文报导了胰腺提取物中两种可被钙／钙调素依赖性蛋白激酶磷酸化的热稳定蛋白。ＳＤＳ－ＰＡＧＥ测定其表观分子量分别为１７．７ｋＤ和６ｋＤ。经钙／钙调素依赖性蛋白激酶磷酸化后,其最大磷酸参入量为８．８μｍｏｌ／ｇ蛋白。同时磷酸化作用导致１７．７ｋＤ蛋白在ＳＤＳ－ＰＡＧＥ中迁移率发生变化。本文还进一步分析了各种阳离子对磷酸化的影响,并对此两种蛋白可能具有的生理功能进行了初步探讨。     

Oncogenes,protein tyrosine kinases,and signal transduction

Many oncogenes encode protein tyrosine kinases (PTKs). Oncogenic mutations of these genes invariably result in constitutive activation of these PTKs. Autophosphorylation of the PTKs and tyrosine phosphorylation of their cellular substrates are essential events for transmission of the mitogenic signal into cells. The recent discovery of the characteristic amino acid sequences, of thesrc homology domains 2 and 3 (SH2 and SH3), and extensive studies on proteins containing the SH2 and SH3 domains have revealed that protein tyrosine-phosphorylation of PTKs provides phosphotyrosine sites for SH2 binding and allows extracellular signals to be relayed into the nucleus through a chain of protein-protein interactions mediated by the SH2 and SH3 domains. Studies on oncogenes, PTKs and SH2/SH3-containing proteins have made a tremendous contribution to our understanding of the mechanisms for the control of cell growth, oncogenesis, and signal transduction. This review is intended to provide an outline of the most recent progress in the study of signal transduction by PTKs.     

Cytogenetic study of mentally retarded children in Taipei

560 blood samples collected from mentally retarded children in Taipei were karyotypically analyzed for the incidence of fragile X and other chromosome abnormalities. The fragile site at Xq27.3 was observed in 18 patients (3.21%), 11 males and 7 females, out of the 560 blood cultures using M medium. Down syndrome (6.25%), 24 males and 11 females, was the other major category of abnormality. Other abnormalities, including inversion, translocation, deletion, duplication, ring as well as an extra marker chromosome were observed. The overall incidence of chromosomal abnormalities in these children was 14.82%.     

pH降低和短杆菌肽D诱发的PE脂质体融合

 ｐＨ降低和短杆菌肽Ｄ诱发的ＰＥ脂质体融合王卓智,聂松青,林克椿（北京医科大学生物物理教研室,北京１０００８３）生物膜的融合是其在执行生理功能时的一种重要现象,如精子与卵子的融合,吞噬细胞形成吞噬体,出胞和入胞,以及病毒感染细胞等,都经历膜融合过程,此...     

广西HBsAg阳性母亲的胎儿肝、肾细胞中乙肝病毒DNA存在状态的研究

采用核酸分子杂交Ｓｏｕｔｈｅｒｎ印迹法,以３２Ｐ标记的ＨＢＶＤＮＡ为探针,检测ＨＢｓＡｇ阳性母亲引产的４０例胎儿的肝、肾组织。结果有２例胎肝和１例胎肾细胞ＤＮＡ出现大于３．２ｋｂ的杂交带,表明ＨＢＶＤＮＡ已处于整合状态。胎肾细胞基因组中查出ＨＢＶＤＮＡ整合为首次报道。     

Phosphorylation and internalization of gp130 occur after IL-6 activation of Jak2 kinase in hepatocytes.

Recent evidence has shown that members of the Jak kinase family are activated after IL-6 binds to its receptor complex, leading to a tyrosine phosphorylation of gp130, the IL-6 signal-transducing subunit. The different members of the IL-6 cytokine subfamily induce distinct patterns of Jak-Tyk phosphorylation in different cell types. Using monospecific antibodies to gp130, Jak2 kinase, and phosphotyrosine, we investigated the kinetics of IL-6 stimulation of members of this pathway in primary hepatocytes. Our findings show that Jak 2 is maximally activated within 2 min of exposure to IL-6, followed by gp130 phosphorylation that reaches its peak in another 2 min then declines to basal level by 60 min. In vitro phosphorylation experiments show that activated Jak 2 is able to phosphorylate both native gp130 and a fusion peptide containing its cytoplasmic domain, demonstrating gp130 is a direct substrate of Jak 2 kinase. Experiments designed to explore the cell surface expression of gp130 show that > or = 2 h are required to get a second round of phosphorylation after the addition of more cytokines. This finding suggests that activated gp130 is internalized from the cell surface after IL-6 stimulation. Additional experiments using protein synthesis inhibitors reveal that new protein synthesis is required to get a second cycle of gp130 phosphorylation indicating gp130 must be synthesized de novo and inserted into the membrane. These findings provide strong evidence that down regulation of the IL-6 signal in hepatocytes involves the internalization and cytosol degradation of gp130.     

Characterization of Rhodobacter capsulatus genes encoding a molybdenum transport system and putative molybdenum-pterin-binding proteins.

The alternative, heterometal-free nitrogenase of Rhodobacter capsulatus is repressed by traces of molybdenum in the medium. Strains carrying mutations located downstream of nifB copy II were able to express the alternative nitrogenase even in the presence of high molybdate concentrations. DNA sequence analysis of a 5.5-kb fragment of this region revealed six open reading frames, designated modABCD, mopA, and mopB. The gene products of modB and modC are homologous to ChlJ and ChlD of Escherichia coli and represent an integral membrane protein and an ATP-binding protein typical of high-affinity transport systems, respectively. ModA and ModD exhibited no homology to known proteins, but a leader peptide characteristic of proteins cleaved during export to the periplasm is present in ModA, indicating that ModA might be a periplasmic molybdate-binding protein. The MopA and MopB proteins showed a high degree of amino acid sequence homology to each other. Both proteins contained a tandem repeat of a domain encompassing 70 amino acid residues, which had significant sequence similarity to low-molecular-weight molybdenum-pterin-binding proteins from Clostridium pasteurianum. Compared with that for the parental nifHDK deletion strain, the molybdenum concentrations necessary to repress the alternative nitrogenase were increased 4-fold in a modD mutant and 500-fold in modA, modB, and modC mutants. No significant inhibition of the heterometal-free nitrogenase by molybdate was observed for mopA mopB double mutants. The uptake of molybdenum by mod and mop mutants was estimated by measuring the activity of the conventional molybdenum-containing nitrogenase. Molybdenum transport was not affected in a mopA mopB double mutant, whereas strains carrying lesions in the binding-protein-dependent transport system were impaired in molybdenum uptake.     

Photolithoautotrophic growth and control of CO2 fixation in Rhodobacter sphaeroides and Rhodospirillum rubrum in the absence of ribulose bisphosphate carboxylase-oxygenase.

Rhodospirillum rubrum and Rhodobacter sphaeroides were shown to be capable of photolithoautotrophic growth in the absence of the reductive pentose phosphate (Calvin) cycle. Ribulose 1,5-bisphosphate carboxylase-oxygenase (RubisCO) deletion strains were incapable of photolithoautotrophic growth using hydrogen as an electron donor but were able to grow in the absence of organic carbon using less reduced inorganic electron donors, i.e., thiosulfate or sulfide. Wild-type R. rubrum grown in the presence of thiosulfate contained RubisCO levels that were 50-fold lower compared with those in cells growth with hydrogen as an electron donor without substantially influencing rates of photolithoautotrophic growth. These results suggest there are two independent CO2 fixation pathways that support photolithoautotrophic growth in purple nonsulfur photosynthetic bacteria, indicating that these organisms have developed sophisticated control mechanisms to regulate the flow of carbon from CO2 through these separate pathways.