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【bio-news】奥克兰儿童医院关于铁调控的新发现
12/21/06 -- A new study co-authored by Children's Hospital Oakland Research Institute (CHORI) senior scientist, Elizabeth Theil, Ph.D., is the first to show that partial copies of DNA called mRNA (or messenger RNA) morph into specific three dimensional shapes when it combines with a protein regulator called IRP1. This discovery is incredibly important to researchers who design medications based on the specific characteristics of a disease.
The study, featured in the December issue of Science, contains some significant surprises about the structure and protein plasticity of IRP1 and the mRNA. Dr. Theil chairs the Council on BioIron at CHORI and is a professor at the University of California, Berkeley. She co-authored the study with William Walden, Ph.D. a professor of microbiology and immunology and his colleague, Karl Voltz, Ph.D., an associate professor at the University of Illinois at Chicago.
The researchers found that when mRNA and IRP1 join they change shapes to fit each other. In addition, the IRP1 changes its role from being an enzyme to an iron regulator. Each mRNA codes one or two proteins in the body. In this case the coded protein was Ferritin, which is essential for managing iron in the body. This discovery could help researchers design medications for patients with iron overload that occurs in hemochromotosis, Sickle Cell Disease and Thalassemia.
"Currently, there are medications available that are based on DNA structures such as anti-cancer drugs. Unfortunately, the problem with targeting DNA is that both healthy and cancerous cells have the same DNA, but they also have different mRNAs. Consequently, our research findings could help scientists design medications that target mRNAs," said Dr. Theil.
Source: Children's Hospital & Research Center at Oakland
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本人认领该文编译，48小时后若未提交译文，请其他战友自由认领。 12/21/06 -- A new study co-authored by Children's Hospital Oakland Research Institute (CHORI) senior scientist, Elizabeth Theil, Ph.D., is the first to show that partial copies of DNA called mRNA (or messenger RNA) morph into specific three dimensional shapes when it combines with a protein regulator called IRP1. This discovery is incredibly important to researchers who design medications based on the specific characteristics of a disease.
根据06年12月21日奥克兰儿童医院研究所的的资深科学家Elizabeth Thei博士和其合作者第一个研究发现，部分DNA的拷贝即mRNA（信使RNA）当结合调节蛋白IRP1时形态将转变成特定的三级结构形式。这项研究结果对于运用该特异性设计疾病药物的研究者来说无疑是非常重要的发现。
The study, featured in the December issue of Science, contains some significant surprises about the structure and protein plasticity of IRP1 and the mRNA. Dr. Theil chairs the Council on BioIron at CHORI and is a professor at the University of California, Berkeley. She co-authored the study with William Walden, Ph.D. a professor of microbiology and immunology and his colleague, Karl Voltz, Ph.D., an associate professor at the University of Illinois at Chicago.
该研究作为12月份《科学》杂志主要内容，在mRNA和IRP1的结构方面有着相当惊人的发现。Theil博士主持在CHORI的生物铁会议并且也是California, Berkeley大学的教授。她和微生物学和免疫学教授、理学博士William Walden及William Walden的同事芝加哥Illinois大学副教授Karl Voltz博士共同研究得到了该结果。
The researchers found that when mRNA and IRP1 join they change shapes to fit each other. In addition, the IRP1 changes its role from being an enzyme to an iron regulator. Each mRNA codes one or two proteins in the body. In this case the coded protein was Ferritin, which is essential for managing iron in the body. This discovery could help researchers design medications for patients with iron overload that occurs in hemochromotosis, Sickle Cell Disease and Thalassemia.
研究者发现当mRNA和IRP1结合时他们的形态变得非常适合双方。此外，IRP1的角色也发生改变即从酶变成铁调节蛋白。每个mRNA编码一个或两个蛋白。当mRNA和IRP1结合时编码铁蛋白，该蛋白在体内是结合铁的蛋白质。该发现能帮助研究者为铁超量疾病镰状红细胞贫血症和地中海贫血〔症〕患者设计药物。
"Currently, there are medications available that are based on DNA structures such as anti-cancer drugs. Unfortunately, the problem with targeting DNA is that both healthy and cancerous cells have the same DNA, but they also have different mRNAs. Consequently, our research findings could help scientists design medications that target mRNAs," said Dr. Theil.
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作者:admin@医学,生命科学 2011-04-07 18:15
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