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resume 代写:DNA

悉尼代写essay

resume 代写:DNA

我们观察到,在离体的DNA中有无烟煤。这是化合物的一个重要功能,它可以在许多领域找到它的应用。它被观察到包括几个晶体结构复合体的DNA。在这种情况下,Doxorubicin (DOX)破坏DNA并干扰DNA合成。这个特殊的功能对于化合物的处理非常重要。这是该化合物具有药理作用的主要原因。据观察,DNA-DOX的相互作用随后导致拓扑异构酶II的中毒(TOP2A)。在细胞核中有DOX的易位,并被认为与蛋白酶体结合。TOP2A毒素介导的细胞毒性与修复基因MSH2和MLH1的失配有关。由于不匹配的偿还功能导致了DNA的丢失。这就导致了阿霉素的耐药性。

resume 代写:DNA
拓扑异构酶II DNA是过程中的损伤,这保证了细胞的死亡。TP53基因是在细胞凋亡和dna损伤反应中起重要作用的基因。这增加了TP53的上调调控,并被发现对蒽环素治疗有影响。ERCC2和TP53通过DOX处理与p53介导的apoptopic通路相互作用。DOX会减少1个电子的数量,形成一个多-半醌基。这些酶包括在肌浆网和线粒体中存在的线粒体NADH脱氢酶。这种化合物的主要限制之一是化合物的毒性和耐药性。该化合物的完全潜力尚未完全分析。

resume 代写:DNA

Anthracyclines is observed intercalate with the DNA in vitro. This is an important functionality of the compound that finds its application in many sectors. It is observed to encompass several crystal structures complexes of the DNA. In this case, the Doxorubicin (DOX) breaks the DNA and interferes with the DNA synthesis. This particular function is very important for the treatment of the compounds. This is the main reason for the compound to have pharmacological uses. It is observed that the DNA-DOX interaction subsequently lead to the poisoning of the topoisomerase II (TOP2A). There is translocation of the DOX into the nucleus and is thought to bind with the proteasomes. The TOP2A poison-mediated cytotoxicity involves itself with the mismatching of the repair genes MSH2 and MLH1. There is a loss of DNA owing to the mismatch repaid functions. This results in the resistance of the doxorubicin.

resume 代写:DNA
Topoisomerase II DNA is damages in the process and this ensures the cell death. TP53, a gene, is the gene that plays an important role in the apoptosis and DNA-damage response. This increases the up regulation of TP53 and is found to impact the anthracycline treatment. The ERCC2 and TP53 interact with the p53-mediated apoptopic pathway with the DOX treatment. The DOX undergoes one-electron reduction and forms a DOX-semiquinone radical. These enzymes include the mitochondrial NADH dehydrogensase that are present in the sarcoplasmic reticulum along with the mitochondria. One of the main limitations for this medicinal compound is the toxicity and resistance of the compounds. The complete potential of the compound is yet to completely analyze.