DNA甲基化模式及其在癌症中的作用

随着对癌症研究的不断深入,表观遗传调控在癌症发生发展中的作用也越来越受到人们的关注。DNA基化作为一种重要的表观遗传修饰机制,在基因表达调控中起着十分重要的作用。该文对DNA基化模式及其在癌症中的作用作了综述,并对DNA甲基化作为癌症早期诊断的生物标记以及癌症表观治疗的新策略作了总结和展望。     

Protein Splicing: How Inteins Escape from Precursor Proteins

Inteins are nature''s escape artists; they facilitate their excision from flanking polypeptides (exteins) concomitant with extein ligation to produce a mature host protein. Splicing requires sequential nucleophilic displacement reactions catalyzed by strategies similar to proteases and asparagine lyases. Inteins require precise reaction coordination rather than rapid turnover or tight substrate binding because they are single turnover enzymes with covalently linked substrates. This has allowed inteins to explore alternative mechanisms with different steps or to use different methods for activation and coordination of the steps. Pressing issues include understanding the underlying details of catalysis and how the splicing steps are controlled.     

Selenium Overcomes Doxorubicin Resistance in Their Nano-platforms Against Breast and Colon Cancers

Biological Trace Element Research - Colon cancer in men and breast cancer in women are regarded as major health burdens, accounting for majority of cancer diagnoses globally. Doxorubicin (DOX)...     

粤东地区野生杜鹃花资源及其开发利用

经调查统计,粤东地区野生杜鹃花有11种．其中．该区特产2种．模式植物2种,主要分布在该区北部山区。在调查的基础上就粤东地区野生杜鹃花资源的开发利用提出建议。     

Oncogene homologues in yeast

Two different yeasts have a number of genes bearing striking structural and functional homologies to mammalian oncogenes. In yeast these genes are involved in the control of proliferation and early steps in the cell cycle. Many have putative protein kinase activity and some have been shown to control the activity of the enzyme adenylate cyclase which synthesizes cyclic AMP. Mutant forms of these yeast genes have oncogenic activity in mammalian cells.     

Oncogene expression in myelopoiesis

Oncogenes are a class of genes hypothesized to be causally related to neoplasia. To date, specific oncogenes have been recognized chiefly by their ability to transform test cells to a neoplastic phenotype. This has been accomplished largely through mutational analysis of the genotype of retroviruses or through the analysis of tumor cell DNA by in vitro transfection of rodent fibroblasts. Oncogenes are believed to arise by some genetic alteration from normal cellular genes called proto-oncogenes. Although the normal function of most proto-oncogenes is unknown, it has been proposed that they may function as tissue-specific and temporally specific regulators of differentiation. The role of oncogenes in lymphoid malignancies has been extensively analyzed. Less is known about their role in myeloid leukemias and especially in normal myelopoiesis. Space limitations permit discussion of only salient features of a limited number of oncogenes; we have arbitrarily selected myc, myb, fos, fms, fes, sis, and abl.     

Reversion and T Cell Escape Mutations Compensate the Fitness Loss of a CD8+ T Cell Escape Mutant in Their Cognate Transmitted/Founder Virus

Immune escape mutations that revert back to the consensus sequence frequently occur in newly HIV-1-infected individuals and have been thought to render the viruses more fit. However, their impact on viral fitness and their interaction with other immune escape mutations have not been evaluated in the background of their cognate transmitted/founder (T/F) viral genomes. To precisely determine the role of reversion mutations, we introduced reversion mutations alone or together with CD8⁺ T cell escape mutations in their unmodified cognate T/F viral genome and determined their impact on viral fitness in primary CD4⁺ T cells. Two reversion mutations, V247I and I64T, were identified in Gag and Tat, respectively, but neither had measurable effect on the fitness of their cognate T/F virus. The V247I and G248A mutations that were detected before and concurrently with the potent T cell escape mutation T242N, respectively, were selected by early T cell responses. The V247I or the G248A mutation alone partially restored the fitness loss caused by the T242N mutation. Together they could fully restore the fitness of the T242N mutant to the T/F level. These results demonstrate that the fitness loss caused by a T cell escape mutation could be compensated by preexisting or concurrent reversion and other T cell escape mutations. Our findings indicate that the overall viral fitness is modulated by the complex interplay among T cell escape, compensatory and reversion mutations to maintain the balance between immune escape and viral replication capacity.     

Escape Behaviour: Reciprocal Inhibition Ensures Effective Escape Trajectory

When a zebrafish makes a fast escape response, Mauthner cells directly activate contralateral spinal interneurons which feed reciprocal inhibition to motorneurons on the stimulated side. Ablation of these interneurons in transgenic animals impairs escape responses, indicating their crucial role in survival.     

How City Dwellers Affect Their Resource Hinterland

This article links databases on household consumption, industrial production, economic turnover, employment, water use, and greenhouse gas emissions into a spatially explicit model. The causal sequence starts with households demanding a certain consumer basket. This demand requires production in a complex supply-chain network of interdependent industry sectors. Even though the household may be confined to a particular geographical location, say a dwelling in a city, the industries producing the indirect inputs for the commodities that the household demands will be dispersed all over Australia and probably beyond. Industrial production represents local points of economic activity, employment, water use, and emissions that have local economic, social, and environmental impacts. The consumer basket of a typical household is followed in Australia's two largest cities—Sydney and Melbourne—along its upstream supply chains and to numerous production sites within Australia. The spatial spread is described by means of a detailed regional interindustry model. Through industry-specific emissions profiles, industrial production is then translated into local impacts. We show that annually a typical household is responsible for producing approximately 80 tonnes of greenhouse gas emissions, uses around 3 million liters of water, causes about A$140,000 to circulate in the wider economy, and provides labor worth just under three full-time employment-years. We also introduce maps that visually demonstrate how a very localized household affects the environment across an entire continent. Our model is unprecedented in its spatial and sectoral detail, at least for Australia.