慢性蜜蜂麻痹病病毒核酸与蛋白质组分的研究

从自然感染的意大利麻痹病蜂(APis mellifera)头部,经二次差速离心与蔗糖梯度离心获得纯化的慢性蜜蜂麻痹病病毒(CBPV)。纯化的CBPV制备物感染正常蜜蜂,4天后出现典型的麻痹症状,接着死亡,平均死亡率分别为95％与100％。SDS-聚丙烯酰胺凝胶电泳分析,二次差速离心初步纯化的病毒制备物含有多条蛋白带,而蔗糖密度梯度纯化的病毒制备物仅含有单一的多肽带。5％、7.5％与10％SDS-聚丙烯酰胺凝胶电泳分析,均检测出一种病毒蛋白质,分子量大约为24,200道尔顿,而且不同凝胶浓度检测的蛋白质分子量相近。慢性蜜蜂麻痹病病毒核酸也用SDS-聚丙烯酰胺凝胶电泳分析,结果表明,凝胶中有5条带,对核酸酶敏感,证明该病毒含有5个单股RNA组分。对慢性蜜蜂麻痹病病毒的基因组结构进行了讨论。     

对氧磷酶研究进展

对氧磷酶（paraoxonase,PON)基因家族至少有三个成员,包括PON1、PON2和PON3。PON1基因产物,也叫血清对氧磷酶,主要在肝脏中表达。作者综述了PON1的性质,催化活性,多态性,及其在有机磷化合物解毒中的重要作用,以及与动脉粥样硬化,冠心病及Ⅱ型糖尿病之间的相关性。还简单介绍了PON2基因多态性与冠心病、血浆脂蛋白和血浆葡萄糖之间的关系。     

黄金树B类MADS-box基因表达特征分析

采用同源克隆技术, 从黄金树(Catalpa speciosa)花芽中克隆得到B类MADS-box基因CaspAP3和CaspPI的cDNA序列。序列分析表明, CaspAP3基因cDNA序列的完整开放阅读框(ORF)为696 bp, 编码231个氨基酸残基; CaspPI基因cDNA序列的ORF为639 bp, 编码212个氨基酸残基。蛋白质序列相似性比对和分子系统发生分析表明, CaspAP3属于AP3/DEF进化支, 其C末端包含保守的euAP3基序和PI-derived基序, 而CaspPI聚类于PI/GLO进化支, 其C末端包含保守的PI基序。半定量RT-PCR分析结果表明, CaspAP3和CaspPI基因均仅在花瓣和雄蕊中表达。实时荧光定量PCR分析表明, CaspAP3和CaspPI基因在花瓣和雄蕊原基分化期至成熟期均有表达, 这2个基因在雄蕊中表达高峰出现的时间均早于花瓣; 且花瓣中的CaspAP3和CaspPI基因表达高峰均出现在快速伸长阶段; 这与花瓣和雄蕊的形态发育阶段相吻合。     

猪产仔数分子标记及其效应分析

初步确定了2个新的猪产仔数分子标记,雌激素受体基因ESR的第8外显子处的ESRB位点、催乳素受体基因的第7外显子的FSHRB位点。通过比较和分析多个产仔数的效应,初步确定了4个有利于产仔数提高的分子标记基因型,基因位点ESR、FSHRB的基因型BB的产仔数显著地高于AB、AA型;位点ESRB、PRLR的基因型AA的产仔数显著地高于AB、BB型;4个基因位点多态性与仔猪生长性能、母猪乳头数不存在显著的影响。     

Activation of STAT6 by STING is critical for antiviral innate immunity

STAT6 plays a prominent role in adaptive immunity by transducing signals from extracellular cytokines. We now show that STAT6 is required for innate immune signaling in response to virus infection. Viruses or cytoplasmic nucleic acids trigger STING (also named MITA/ERIS) to recruit STAT6 to the endoplasmic reticulum, leading to STAT6 phosphorylation on Ser(407) by TBK1 and Tyr(641), independent of JAKs. Phosphorylated STAT6 then dimerizes and translocates to the nucleus to induce specific target genes responsible for immune cell homing. Virus-induced STAT6 activation is detected in all cell-types tested, in contrast to the cell-type specific role of STAT6 in cytokine signaling, and Stat6(-/-) mice are susceptible to virus infection. Thus, STAT6 mediates immune signaling in response to both cytokines at the plasma membrane, and virus infection at the endoplasmic reticulum.     

Characterization and utilization of methyltransferase for apramycin production in Streptoalloteichus tenebrarius

A structurally unique aminoglycoside produced in Streptoalloteichus tenebrarius, Apramycin is used in veterinary medicine or the treatment of Salmonella, Escherichia coli, and Pasteurella multocida infections. Although apramycin was discovered nearly 50 years ago, many biosynthetic steps of apramycin remain unknown. In this study, we identified a HemK family methyltransferase, AprI, to be the 7’-N-methyltransferase in apramycin biosynthetic pathway. Biochemical experiments showed that AprI converted demethyl-aprosamine to aprosamine. Through gene disruption of aprI, we identified a new aminoglycoside antibiotic demethyl-apramycin as the main product in aprI disruption strain. The demethyl-apramycin is an impurity in apramycin product. In addition to demethyl-apramycin, carbamyltobramycin is another major impurity. However, unlike demethyl-apramycin, tobramycin is biosynthesized by an independent biosynthetic pathway in S. tenebrarius. The titer and rate of apramycin were improved by overexpression of the aprI and disruption of the tobM2, which is a crucial gene for tobramycin biosynthesis. The titer of apramycin increased from 2227 ± 320 mg/L to 2331 ± 210 mg/L, while the titer of product impurity demethyl-apramycin decreased from 196 ± 36 mg/L to 51 ± 9 mg/L. Moreover, the carbamyltobramycin titer of the wild-type strain was 607 ± 111 mg/L and that of the engineering strain was null. The rate of apramycin increased from 68% to 87% and that of demethyl-apramycin decreased from 1.17% to 0.34%.     

干细胞在肝脏疾病治疗中的临床应用及分子机制

干细胞是指一群具有自我更新和多向分化潜能的细胞,是最有治疗潜力的细胞资源,已成为再生医学领域的研究热点。目前,已有多种干细胞用于肝脏疾病的治疗,能有效改善患者血清指标,减少并发症发生,并提高生活质量。这些干细胞在细胞来源、移植途径及治疗效果等多个方面各有特点,但其治疗肝脏疾病的机制尚不清楚。本文将对目前已用于肝病治疗的各种干细胞的临床应用以及可能的分子机制进展进行阐述。     

BMP2/7 heterodimer enhances osteogenic differentiation of rat BMSCs via ERK signaling compared with respective homodimers

Bone morphogenetic protein (BMP)2/7 heterodimer shows greater efficacy in enhancing bone regeneration. However, the precise mechanism and the role of mitogen-activated protein kinase (MAPK) signaling network in BMP2/7-driven osteogenesis remain ambiguous. In this study, we evaluated the effects of BMP2/7 heterodimers on osteoblastic differentiation in rat bone marrow mesenchymal stem cells (BMSCs), with the aim to elaborate how MAPKs might be involved in this cellular process by treatment of rat BMSCs with BMP2/-7 with a special signal-pathway inhibitor. We found that BMP2/7 heterodimer induced a much stronger osteogenic response in rat BMSCs compared with either homodimer. Most interestingly, extracellular signal-regulated kinase (ERK) demonstrated a highly sustained phosphorylation and activation in the BMP2/7 heterodimer treatment groups, and inhibition of ERK cascades using U0126 special inhibitor that significantly reduced the activity of ALP and calcium mineralization to a substantial degree in rat BMSCs treated with BMP2/7 heterodimers. Collectively, we demonstrate that BMP2/7 heterodimer shows a potent ability to stimulate osteogenesis in rat BMSCs. The activated ERK signaling pathway involved in this process may contribute partially to an increased osteogenic potency of heterodimeric BMP2/7 growth factors.