In memoriam: Professor Ray WU

<正>During the Chinese New Year holidays in 2008, Professor Zhang Nai-Heng, former chair of the Department of Biochemistry, Beijing Medical College, informed me of the sad news that Professor Ray Wu had passed away in Ithaca, New York on     

神经生长因子家族及其受体研究进展

过去几年在神经营养因子、受体和神经元细胞程序性死亡的研究领域中取得了几项引人注目的进展：（１）神经生长因子（ＮＧＦ）基因家族的其他一些成员包括脑源性神经营养因子（ＢＤＮＦ）、神经营养素－３（ＮＴ－３）、神经营养素－４（ＮＴ－４）、神经营养素－５（ＮＴ－５）的发现;（２）神经生长因子三维结构及功能和进化之关系的阐明;（３）定性了两种神经生长因子受体Ｐ７５＾ＮＧＦＲ和原癌基因ｐ１４０＾ｔｒｋＡ以及相关     

中国杏属一新种

描述了中国杏属一新种,华仁杏(Armeniaca cathayanaD.L.Fu,B.R.Li et J.H.Li,sp.nov.)。该新种与杏(Armeniaca vulgarisLam.)和山杏(A.sibirica(L.)Lam.)相似,但又有其独特特征,主要区别如下:叶两面疏被短柔毛,边缘具单锯齿和重锯齿,基部全缘;叶柄无腺体;单花或2~3朵花簇生;子房密被白色长柔毛;果核三角状卵球形,腹缝线具5~7条锐纵棱,背缝线具1条浅纵沟;种子大,两侧压扁,种仁质脆,无苦味。该新种由傅大立于2008年7月11日在河北省涿鹿县发现并采集,模式标本存于中国林业科学研究院(CAF),标本号:No.2008071101。     

人神经生长因子低亲和力受体（p~（75）NGFR）cDNA的克隆及其在神经细胞中表达活性的初步研究

利用酸性异硫氰酸胍－酚－氯仿一步法从人胎儿基底前脑中提取总ＲＮＡ,用逆转录与聚合酶链反应相结合的ＲＴ－ＰＣＲ法,扩增出人神经生长因子低亲和力受体ｐ~（７５）ＮＧＦＲ基因ｃＤＮＡ,在限制性内切酶ＳｍａⅠ存在下的连接体系中,将扩增出的ｃＤＮＡ片段克隆入ｐＵＣ１２的ＳｍａⅠ位或,经限制性内切酶ＥｃｏＲⅠ和ＰｓｔⅠ酶切鉴定是否插入以及ＨｉｎｄⅢ酶切鉴定方向。将重组质粒中的ｐ~（７５）ＮＧＦＲ的ｃＤＮＡ再次亚克隆至ｐＵＣ１２载体中后,以其双链ＤＮＡ为模板,用末端终止法测出其全部核苷酸顺序,证实其核苷酸编码的ｐ~（７５）ＮＧＦＲ除两个碱基突变外,其余与文献完全一致。完整的ｐ~（７５）ＮＧＦＲ的ｃＤＮＡ分两步克隆到逆转录病毒表达载体ｐＸＴ－１,经ＰＡ３１７包装细胞株体外包装后、收集病毒上清转染条件不死性大鼠小脑神经细胞系Ｒ２．初步结果表明转染了ｐ~（７５）ＮＧＦＲ的Ｒ２细胞株去除ＮＧＦ培养时出现程序化死亡的典型特征梯型ＤＮＡ带。     

乙型肝炎病毒X基因的分析与在大肠杆菌中的表达

以ＨＢＶ－ＮＣｌＤＮＡ为材料研究了其中的Ｘ基因,首先确定了此Ｘ基因的顺序,即用ＡＢＩ自动萤光测序议测序证明了此Ｘ基因的３８５位核苷酸后缺失１９个核苷酸,从而引起移码突变,使此Ｘ基因共有５１９个核苷酸,编码１７２个氨基酸,比另一种ａｄｒ型Ｘ蛋白多１８个氨基酸。在其第五位氨基酸上有一ＡＴＧ起始密码,也与另一Ｘ基因不同。经重组后获得在大肠杆菌中的热诱导表达,用Ｗｅｓｔｅｒｎｂｌｏｔ方法证明确为Ｘ蛋白,并有多态性。     

Persistent Translocation of Ca2+/Calmodulin-Dependent Protein Kinase II to Synaptic Junctions in the Vulnerable Hippocampal CA1 Region Following Transient Ischemia

Abstract: The influence of brain ischemia on the subcellular distribution and activity of Ca²⁺/calmodulin-dependent protein kinase II (CaM kinase II) was studied in various cortical rat brain regions during and after cerebral ischemia. Total CaM kinase II immunoreactivity (IR) and calmodulin binding in the crude synaptosomal fraction of all regions studied increase but decrease in the microsomal and cytosolic fractions, indicative of a translocation of CaM kinase II to synaptosomes. The translocation of CaM kinase II to synaptic junctions occurs but not to synaptic vesicles. The translocation in neocortex and CA3/DG (dentate gyrus) is transient, whereas in the hippocampal CA1 region, it persists for at least 1 day of reperfusion. The Ca²⁺/calmodulin-dependent activity of CaM kinase II in the subsynaptosomal fractions of neocortex is persistently decreased by up to 85%, despite the increase in CaM kinase II IR. The decrease in activity is more pronounced than the decline in IR, suggesting that CaM kinase II is covalently modified in the postischemic phase. The persistent translocation of CaM kinase II in the vulnerable ischemic CA1 region indicates that a pathological process is sustained in the area after the reperfusion phase and this may be of significance for ischemic brain injury.     

电压门控钠离子通道与恶性肿瘤的转移

电压门控钠离子通道(VGSC)是可兴奋组织中动作电位的关键离子通道,具有重要的生理功能.近年来国内外研究发现,VGSC在转移的前列腺癌、乳腺癌、卵巢癌、宫颈癌等细胞中表达,其增加了癌细胞的运动和侵袭,促使了癌症的转移,其还将被作为治疗靶点而进行药物开发和临床应用.     

RanBPM is a novel binding protein for p75NTR

The neurotrophin receptor p75NTR can induce signal transduction both in vivo and in vitro. The mechanisms by which p75NTR transduces signals have remained mostly unknown. Using yeast two-hybrid system, we identified the Ran-binding protein (RanBPM) as an interactor with the intracytoplasmic domain of p75NTR (p75ICD). The interaction was then validated by immunoprecipitation in mammalian cells and immunoblotting analysis. The domain in p75ICD interacting with RanBPM was mapped to the death domain.     

eIF4A1与TrkA相互作用后抑制TrkA的泛素化

神经生长因子（NGF）结合细胞表面受体p75NTR(p75神经营养素受体)和TrkA（酪氨酸蛋白激酶A）后介导了细胞分化、细胞生存、凋亡、增殖和侵袭等多个重要的生理病理过程. TrKA能与细胞内多个蛋白质相互作用,但是由于NGF信号通路的复杂性,现在仍有必要发现与之相互作用的蛋白质以更准确地了解NGF信号通路. 本研究中我们通过酵母双杂交的方法筛选到了一个新的与TrKA相互作用的蛋白质——真核生物翻译起始因子4A1（eIF4A1）,然后通过谷胱甘肽巯基转移酶融合蛋白沉降实验（GST-pull-down）和免疫共沉淀实验（Co-IP）证明了TrkA和eIF4A1的相互作用. 此外NGF能够增强TrkA和eIF4A1的相互作用. 在鉴定相互作用位点实验中,我们发现eIF4A1的氨基端结构域和TrkA的TK结构域参与了相互作用. TrkA和eIF4A1共定位在细胞膜上. NGF能够引起TrkA与泛素蛋白63位的赖氨酸连接,而eIF4A1与TrkA相互作用后能够抑制TrkA与泛素蛋白63位的赖氨酸连接. 综上,得出结论 eIF4A1通过与TrkA相互作用抑制其泛素化调控NGF信号通路.     

维生素D受体最新研究进展

维生素D受体(vitamin D receptor,VDR)是一种核转录因子,通过与配体特异结合,调控多种基因的表达,从而调节多种生命活动的进行.本文总结了近年来VDR的研究进展,主要包括VDR的作用机制、VDR行使功能所需共激活子及共抑制子、VDR在生长分化、免疫调节和抑制肿瘤等方面的作用及VDR配体类似物在药物开发研究领域的最新进展.