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Article #279Post-Docs.com ==> Disease-Associated Defects in RNA Metabolism
From: mydj2003
Date: Thu, 16 Nov 2000 00:00
Date: Thu, 16 Nov 2000 00:00
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4051 bytes
------------------------------------------------------- Selected job posting: Postdoctoral position posted on post-doctoral website: http://www.post-docs.com -------------------------------------------------------- Post-doctoral position in Disease-Associated Defects in RNA Metabolism Categories: Agriculture and Life Sciences Medicine and Health Sciences Date Posted: 11/16/2000 Contact: Professor Lynne E. Maquat University of Rochester School of Medicine and Dentistry Biochemistry and Biophysics Rochester, NY 14642 USA Telephone: 716-273-5640 Fax: 716-271-2683 Postdoctoral Positions in Disease-Associated Defects in RNA Metabolism Postdoctoral positions are available to study the mechanism by which nonsense codons elicit mRNA decay in mammalian cells. Nonsense codons, caused by either frameshift or nonsense mutations, are responsible for an estimated one-third of inherited genetic diseases. If the resulting premature termination of translation can be abrogated even slightly so as to increase the amount of full-length protein synthesized, then the abnormal phenotypes of many diseases can be abrogated. Therefore, an understanding of nonsense-mediated decay (NMD) is critical to the development of clinically useful therapies. Currently, we are interested in understanding how nuclear pre-mRNA processing and other nuclear events influence mRNP structure in ways that impact cytoplasmic mRNA translation and, in so doing, NMD. Studies will focus on various splicing and translational factors that we have already found influence, respectively, mRNP structure and NMD in order to establish how these factors interact and function (see, e.g., Sun and Maquat, 2000, RNA 6:1-6; Le Hir et al., 2000, Genes & Dev. 14:1098- 1108; Sun, Moriarty, and Maquat, 2000, EMBO J, 19:4734-4744). Interestingly, some of the translational factors derive from alternatively spliced pre-mRNAs so that different isoforms may have different interactive capabilities and, therefore, different roles in NMD. Having demonstrated that NMD involves a PI 3-kinase-related kinase signaling pathway, we are currently pursuing studies of the putative kinase and its modifiers. We are also interested in understanding why certain nonsense-containing mRNAs are immune to NMD decay as well as the mechanisms that specify two distinct cellular sites for NMD. Significant projects are available in molecular biology, biochemistry and cell biology. Successful candidates will join a well-equipped group of interactive lab members with diverse backgrounds and expertise in newly remodeled labs. The University of Rochester is unique for its sizeable community of RNA researchers and its interest in clinical approaches to modify disease-associated gene expression by modifying RNA metabolism. ---------------------------------------- Search hundreds of postdoctoral jobs at http://www.Post-docs.com ----------------------------------------- Sent via Deja.com http://www.deja.com/ Before you buy.
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X-Google-Language: ENGLISH,ASCII-7-bit X-Google-Thread: f9856,d521b4f9ad8386ba,start X-Google-Attributes: gidf9856,public X-Google-Thread: f5161,d521b4f9ad8386ba,start X-Google-Attributes: gidf5161,public X-Google-Thread: f8886,d521b4f9ad8386ba,start X-Google-Attributes: gidf8886,public From: mydj2003@my-deja.com Subject: Post-Docs.com ==> Disease-Associated Defects in RNA Metabolism Date: 2000/11/16 Message-ID: <8v12g5$iea$1@nnrp1.deja.com> X-Deja-AN: 694379866 X-Http-User-Agent: Mozilla/4.0 (compatible; MSIE 5.0; Windows NT; DigExt) X-Complaints-To: news@net.bio.net X-Trace: niobium.hgmp.mrc.ac.uk 974392705 26896 193.62.192.80 (16 Nov 2000 16:38:25 GMT) X-Http-Proxy: 1.1 x63.deja.com:80 (Squid/1.1.22) for client 35.8.121.118 Organization: Deja.com - Before you buy. X-Article-Creation-Date: Thu Nov 16 16:37:26 2000 GMT X-MyDeja-Info: XMYDJUIDmydj2003 NNTP-Posting-Date: 16 Nov 2000 16:38:25 GMT Newsgroups: sci.research.postdoc,sci.research.careers,bionet.jobs