赤轮加冕，紫外线、狂摧乱剪。 蛋白质、支离凋落，何况螺旋双链！ 碱基怜、添补缺失，张冠李戴皆凶险。 见差若毫厘，许仙悲叹，忍看娇妻蛇变。 杞天虑、神医觅，尊号问，名酶是鉴。 侦巡单链错，抽刀了断，碱基再配无亏欠。 记牢模板，尽狸猫扬弃，宸妃太子重依恋。 基因复旧，共赏骄阳艳艳。 烈日下，太阳发出的紫外线照射人体裸露的皮肤，皮肤细胞的一些蛋白质和 DNA 吸收了紫外线，被紫外线破坏了氢键等结构，导致结构改变。 DNA 的遗传信息写在碱基的排列顺序上，一旦 DNA 上面的碱基（核苷酸）出现了增添、缺失或替换， DNA 上面的遗传信息就很有可能被改写，这就是基因突变的分子机制。 遗传信息一旦被改变，就会影响生物性状的表达，而一个碱基的改变却可能会影响整个遗传信息，夸张点说，就像当年白素贞喝了雄黄酒变回了白蛇一样！由于生物目前的稳态是几亿年来自然选择的结果，一旦出现新的性状，往往难以适应当前的环境。所以大多数的基因突变都是有害的，例如癌症、遗传病、死胎、怪胎等。 除了紫外线，还有很多内外的因素如电离辐射、骤冷骤热、内环境酸碱度、细胞分裂等会导致基因突变，那么我们是不是束手待毙呢？其实不然，在细胞里有很多酶，会及时将受损的 DNA 链修复。 2015 年诺贝尔化学奖就授予了三位在揭示 DNA 修复机制做出了卓越贡献的科学家。 当 DNA 的某些碱基或核苷酸出现问题，如胞嘧啶 (C) 脱氨基变成尿嘧啶 (U) 、胸腺嘧啶形成胸腺嘧啶二聚体等错误的时候，这些修复酶就会识别出错误的碱基或核苷酸，单独或将与错误碱基相邻的若干核苷酸一起切除，然后再根据碱基互补配对原则将这条单链修复。当复制时薪形成的子链出现碱基对错配的时候，另一种能识别模板母链的酶根据模板链的序列，将配对错误的子链碱基切除掉，再由碱基互补配对原则进行修复，休想狸猫换太子！ 当然DNA的修复机制还有很多，但不管如何，正是仰仗了这一机制，我们才能在阳光下茁壮成长；也正是揭示了这一机制，我们才有信心最终攻克癌症等由基因引发的绝症！
颁奖典礼上，几个北欧人好像把DNA修复说成很简单的事情：无论是紫外，还是吸烟带来的DNA破坏，人体都有机制修复它。问题是，很多人就是因为紫外或者吸烟获得皮肤癌或者肺癌。 他们的视频可能误导多少烟鬼啊！ DNA修复的局限性没有被观众问到，而2个来自中国的记者浪费时间问了2个答案明显的问题。哪个单位的？ 对DNA修复机制的局限性深入研究，也许能帮助人们寻找治疗癌症等疾病的良药。或许导致以后获得炸药奖。 【补充：倒是其官方资料提及DNA修复的局限和相关的药物研发。】 http://www.nobelprize.org/nobel_prizes/chemistry/laureates/2015/popular-chemistryprize2015.pdf 。。。 Our genome would collapse without these repair mechanisms. If just one component fails, the genetic information changes rapidly and the risk of cancer increases. Congenital damage to the nucleotide excision repair process causes the disease xeroderma pigmentosum; individuals who suffer from this disease are extremely sensitive to UV radiationand develop skin cancer after exposure to the sun. Defects in DNA mismatch repair increase the risk ofdeveloping hereditary colon cancer , for instance.In fact, in many forms of cancer, one or more of these repair systems have been entirely or partiallyswitched off. This makes the cancer cells’ DNA unstable, which is one reason why cancer cells oftenmutate and become resistant to chemotherapy. At the same time, these sick cells are even more dependenton the repair systems that are still functioning; without these, their DNA will become too damaged and thecells will die. Researchers are attempting to utilise this weakness in the development of new cancer drugs.Inhibiting a remaining repair system allows them to slow down or completely stop the growth of the cancer. One example of a pharmaceutical that inhibits a repair system in cancer cells is olaparib . ( https://en.wikipedia.org/wiki/Olaparib )
Department of Biochemistry Molecular Biology at the University of Miami Miller School of Medicine invites applications for a postdoctoral position to study the mechanism of human DNA interstrand cross-link repair that is linked to drug resistance and a cancer-prone syndrome called Fanconi anemia.We employ state-of-the-art techniques such as in vitro biochemical reconstitution, confocal microscopy, flow cytometry, and etc as our research tools.The appointment will be for a period of one year with an option for renewal based on satisfactory performance and availability of the research fund.The incumbent is expected to be a team player to further their personal training as well as collaborative research efforts.The successful applicants must hold a doctoral degree in biochemistry, molecular biology, cell biology, or related areas. Applicants with background in DNA metabolism will receive favorable consideration. The start salary in US dollars will be around $40,000/year depending on experience.Application package including a cover letter, curriculum vitae, contact info of three referees should be sent,preferentiallythrough E-mail,to Dr. Yanbin Zhangat the Department of Biochemistry Molecular Biology, University of Miami Miller School of Medicine, Gautier Bldg/Rm 310, 1011 NW 15 th Street, Miami, FL 33136. 本广告有些措词来自 贺震 博士 ，已经征得博主同意。
首届中德DNA修复与人类疾病研讨会在京举行 http://news.sciencenet.cn/htmlnews/2010/10/238842.shtm http://www.gopubmed.org/web/gopubmed/1?WEB0aspgmmtwxvvsI9I1I00h001000j100200010 7,128 of 23,372 documents semantically analyzed Term: DNA Repair Description: The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as dark repair because they do not require light. Synonyms: Nucleotide Excision Repairs, Nucleotide Excision Repair, Base Excision Repair, Excision Repairs, Base Excision Repairs, Excision Repair 1 2 3 Top Years Publications 2009 550 2007 501 2006 488 2010 482 2008 451 2005 450 2004 422 2003 404 2001 327 2002 299 2000 254 1999 238 1998 190 1996 167 1995 160 1997 158 1991 152 1994 145 1993 136 1992 116 1 2 3 1 2 3 4 Top Countries Publications USA 2,782 United Kingdom 575 Japan 375 Germany 342 France 295 Canada 271 Italy 218 Netherlands 173 Spain 114 China 108 Poland 94 Australia 82 India 72 Brazil 68 Sweden 67 South Korea 62 Switzerland 61 Israel 55 Russia 52 Denmark 50 1 2 3 4 1 2 3 ... 35 Top Cities Publications New York City 164 Boston 159 Houston 146 Bethesda 140 London 105 Baltimore 93 Philadelphia 91 Los Angeles 82 Cambridge, USA 67 Chapel Hill 66 Tokyo 64 Milan 59 Leiden 58 Brighton 57 Stanford 57 Cambridge 55 Paris 50 Rome 49 Seattle 46 San Diego 46 1 2 3 ... 35 1 2 3 ... 48 Top Journals Publications Mutat Res-fund Mol M 610 Cancer Res 274 J Biol Chem 261 Radiat Res 250 Dna Repair 194 Mol Cell Biol 165 P Natl Acad Sci Usa 165 Nucleic Acids Res 154 J Bacteriol 151 Int J Radiat Biol 149 Oncogene 147 Carcinogenesis 143 Cell Cycle 119 Embo J 82 Environ Mol Mutagen 74 Int J Radiat Biol Relat Stud Phys Chem Med 74 Mutagenesis 70 Mol Cell 68 Int J Radiat Oncol 65 Nature 64 1 2 3 ... 48 1 2 3 ... 769 Top Terms Publications DNA Repair 6,646 DNA 6,571 DNA Damage 5,971 DNA repair 4,619 Humans 3,909 Proteins 2,954 Animals 2,810 Genes 2,504 Mutation 2,066 Radiation 1,821 damaged DNA binding 1,727 Cell Cycle 1,657 Cell Line 1,584 DNA-Binding Proteins 1,379 cell cycle 1,367 DNA replication 1,300 Dose-Response Relationship, Radiation 1,294 DNA Breaks 1,282 Genome 1,282 Genomics 1,273 1 2 3 ... 769 1 2 3 ... 1110 Top Authors Publications Iliakis G 35 Jeggo P 34 Bohr V 28 Kaina B 27 Barb J 27 Woodgate R 26 Walker G 25 Samson L 25 Little J 24 Chen D 23 Blasiak J 23 Goodman M 22 Hoeijmakers J 22 Elledge S 22 Fornace A 21 Kinsella T 20 Lbrich M 19 Mullenders L 19 Raaphorst G 19 Weichselbaum R 19 1 2 3 ... 1110
标签: DNA修复
