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Theory of Carbon Signaling. Negentropy vs Entropy - Emergence of Self Propagated Biological Systems

机译:碳信号传导理论。加入和熵 - 自宣传生物系统的出现

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How can we model the causative force of reversible covalent modifications? DNA provides information for synthesizing proteins which in term drive metabolic processes. Understanding basic metabolic processes currently do not help explain regulative forces controlling gene expression. Rather it is claimed that the chromatin state determined by DNA and histone modifications regulate gene expression. We now know that chemistry underlines and explains biological phenomena. However, understanding dynamic chemistry in large space such as a cell has been difficult through conventional models capturing structural changes of metabolites in spatially defined motifs where active sites determine change of mass. How do we expand in space? We certainly need to implement defined physical concepts and to elaborate on set of principles in order to construct emergent principles. The results from sequencing technology have posed new questions that require alternative approaches of system analysis. The functions of non-coding RNA's have linked gene expression with the smallest covalent modifications, methylation and acetylation. The smallest and the largest molecules such as protein complexes are the most difficult to study in biological systems because of their transient characteristics. Hierarchical time scale differences additionally complicate computational models as open systems tend to be difficult to analyze due to environmental, transport, irreversible, or regulatory constrains. Building a dynamic model of multiple dimensional composite functions at each moment by approximating negativity as a function of mass change is what may be necessary for discovering the causative force underlying oscillations in concentrations and states of small molecules and therefore populations. Is there a mechanism to define species' variability through the physics of small molecules relative to the origin of carbon signaling?
机译:我们如何建模可逆的共价修改的致原因? DNA提供了合成蛋白质的信息,该蛋白质在术语驱动代谢过程中。了解基本的代谢过程目前没有帮助解释控制基因表达的规范力。相反,据称是通过DNA和组蛋白修饰测定的染色质状态调节基因表达。我们现在知道化学强调并解释了生物现象。然而,在大型空间中了解在诸如电池的大型空间中的动态化学通过常规模型捕获在空间定义的基序中代谢物的结构变化的结构变化,其中有源网站确定质量变化。我们如何在空间中扩展?我们当然需要实施定义的物理概念,并详细阐述了一组原则,以构建新的原则。测序技术的结果提出了新的问题,需要系统分析的替代方法。非编码RNA的功能具有与最小共价修饰,甲基化和乙酰化的链接基因表达。由于其瞬态特征,最小和蛋白质复合物如蛋白质复合物的最小分子最难以研究生物系统。分层时间尺度差异另外复杂化计算模型作为开放系统由于环境,运输,不可逆转或监管约束而难以分析。通过近似作为质量变化的函数来构建各时刻多维复合功能的动态模型是发现浓度和小分子状态下的造成力和群体的原因和群体的造成力可能所必需的。是否有机制可以通过相对于碳信号传导的来源来定义物种通过小分子的物理学的可变性?

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