携带p53和p21基因腺病毒转移载体的构建

构建携带p53和p21基因的重组腺病毒转移载体以研究p53和p21联合基因治疗效果.将p53cDNA克隆到转移载体pCMV5GFP替代gfp,得到pCMVp53,使其受到CMV启动子的调控;同时将p21基因克隆到pCMVp53,得到重组腺病毒转移载体pCMVp53/p21.得到携带p53和p21基因的重组腺病毒转移载体.     

Splicing factor Sub2p is required for nuclear mRNA export through its interaction with Yra1p.

The yeast nuclear protein Yra1p is an essential export factor for mRNA. Yra1p interacts directly with the mRNA transport factor Mex67p/Mtr2p, which is associated with the nuclear pore. Here, we report a genetic interaction between YRA1 and SUB2, the gene for a DEAD box helicase involved in splicing. Mutation of SUB2 as well as its overexpression leads to a defect in mRNA export. Moreover, Yra1p and Sub2p bind directly to each other both in vivo and in vitro. Significantly, Sub2p and Mex67p/Mtr2p bind to the same domains of Yra1p, and the proteins compete for binding to Yra1p. Together, these data indicate that the spliceosomal component Sub2p is also important in mRNA export and may function to recruit Yra1p to the mRNA. Sub2p may then be displaced from Yra1p by the binding of Mex67p/Mtr2p, which participates in the export of mRNA through the nuclear pores.     

复区域上线性微分方程解的振荡结果

考虑二阶微分方程f ″+[exp(P1)+exp(P 2)+Q(z)]f=0,这里P1=p1zn+…,P2=p2zn+…是非常数多项式,Q(z)是阶小于 n的整函数, 该文研究当-1＜p2/p1＜0时,方程解的振荡结果.     

对溴偶氮氯胂离解作用的研究

用分光光度法和电位滴定法分别测定了对溴偶氮氯胂的六级离解常数 ,其值分别为 :pK1=1 10 ,pK2 =1 34,pK3 =3 4 4 ,pK4 =6 6 7,pK5=9 2 3,pK6=11 84 (分光光度法 ,572nm) ;pK3 =3 32 ,pK4 =6 72 ,pK5=9 89,pK6=11 6 1(电位滴定法 ) .     

Neurotoxicity induces cleavage of p35 to p25 by calpain

Cyclin-dependent kinase 5 (cdk5) and its neuron-specific activator p35 are required for neurite outgrowth and cortical lamination. Proteolytic cleavage of p35 produces p25, which accumulates in the brains of patients with Alzheimer's disease. Conversion of p35 to p25 causes prolonged activation and mislocalization of cdk5. Consequently, the p25/cdk5 kinase hyperphosphorylates tau, disrupts the cytoskeleton and promotes the death (apoptosis) of primary neurons. Here we describe the mechanism of conversion of p35 to p25. In cultured primary cortical neurons, excitotoxins, hypoxic stress and calcium influx induce the production of p25. In fresh brain lysates, addition of calcium can stimulate cleavage of p35 to p25. Specific inhibitors of calpain, a calcium-dependent cysteine protease, effectively inhibit the calcium-induced cleavage of p35. In vitro, calpain directly cleaves p35 to release a fragment with relative molecular mass 25,000. The sequence of the calpain cleavage product corresponds precisely to that of p25. Application of the amyloid beta-peptide A beta(1-42) induces the conversion of p35 to p25 in primary cortical neurons. Furthermore, inhibition of cdk5 or calpain activity reduces cell death in A beta-treated cortical neurons. These observations indicate that cleavage of p35 to p25 by calpain may be involved in the pathogenesis of Alzheimer's disease.     

关于正规约数和函数的Graham问题

设n是大于 1且适合s(n) =[n/2 ]的正整数 ,其中s(n)是n的正规约数和函数 ;ω(n)是n的不同素因数的个数 ,p1,p2 ,… ,pω(n) 是n的适合p1相似文献   

DDT污染土壤的修复技术

采用超声-微波协同技术对实际双对氯苯基三氯乙烷(DDT)污染土壤进行修复,考察水相介质、碱浓度、水投加量、微波电功率、反应时间对DDT去除效果的影响。结果表明:这种修复技术可以有效地去除污染土壤中的2,2-双(4-氯苯基)-1,1,1-三氯乙烷(p,p’-DDT)和二氯二苯二氯代甲烷(p,p’-DDD),降低土壤的毒性。碱性介质的投加更有利于DDT污染土壤毒性的降低,对于20 g污染土壤,最佳碱浓度为6 mol/L;最佳水投加量为4 mL;电功率的提高,不仅可以提高p,p’-DDT、p,p’-DDD的去除效果,还可以去除p,p’-DDT、p,p’-DDD在降解过程中生成的2,2-双(4-氯苯基)-1,1,1-二氯乙烯(p,p’-DDE);最优反应时间为4 min。     

p63 and p73 are required for p53-dependent apoptosis in response to DNA damage

The tumour-suppressor gene p53 is frequently mutated in human cancers and is important in the cellular response to DNA damage. Although the p53 family members p63 and p73 are structurally related to p53, they have not been directly linked to tumour suppression, although they have been implicated in apoptosis. Given the similarity between this family of genes and the ability of p63 and p73 to transactivate p53 target genes, we explore here their role in DNA damage-induced apoptosis. Mouse embryo fibroblasts deficient for one or a combination of p53 family members were sensitized to undergo apoptosis through the expression of the adenovirus E1A oncogene. While using the E1A system facilitated our ability to perform biochemical analyses, we also examined the functions of p63 and p73 using an in vivo system in which apoptosis has been shown to be dependent on p53. Using both systems, we show here that the combined loss of p63 and p73 results in the failure of cells containing functional p53 to undergo apoptosis in response to DNA damage.