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By Allen. Arthur Ormiston

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Cortical as well as cerebellar granule neurons from mutant mice will also be cultured and methods to restore MeCP2 function will be explored. ; Professor and Investigator; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 770303498 Timing: Fiscal Year 2005; Project Start 23-JUL-2001; Project End 31-MAY-2007 Summary: The X-linked neurodevelopmental disorder Rett syndrome (RTT) is one of the leading causes of mental retardation (MR) and autism in females. 80% of girls with RTT have mutations in the gene encoding methyl-CpG- binding protein 2 (MeCP2), a transcriptional repressor that binds methylated cytosines.

Diseases such as Alzheimer's and Rett Syndrome occur when this homeostasis is disrupted. One particular receptor, the NMDA receptor, is important for proper functioning of the synapse. My preliminary studies suggest that snapin forms a complex with the NMDA receptor subunit NR1 and decreases the number of NR1 clusters per unit area of dendrite in hippocampal neurons. Therefore, it is important to understand how this interaction occurs and how it affects functional NMDA receptor trafficking. Our first set of experiments will determine which portion of snapin interacts with NR1 and which splice variant of NR1 interacts with snapin.

Db=pubmed&cmd=Retrieve&dopt=A bstractPlus&list_uids=17101000&query_hl=14&itool=pubmed_docsum 7 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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Advanced examples in physics by Allen. Arthur Ormiston


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