By Philip M. Parker
In March 2001, the nationwide Institutes of wellbeing and fitness issued the next caution: "The variety of sites delivering health-related assets grows on a daily basis. Many websites offer important details, whereas others could have info that's unreliable or misleading." moreover, as a result swift bring up in Internet-based details, many hours should be wasted looking, determining, and printing. in view that simply the smallest fraction of knowledge facing Huntington ailment is listed in se's, resembling www.google.com or others, a non-systematic method of net learn will be not just time eating, but in addition incomplete. This e-book was once created for doctors, scholars, and participants of most people who are looking to behavior clinical study utilizing the main complicated instruments on hand and spending the smallest amount of time doing so.
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Extra info for Huntington Disease - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers
Specific Aim 3 tests the hypothesis that interference in Sp 1 function by huntingtin causes abnormal histone modification. Histone modifications will be examined in mouse and cell models of HD. Taken Studies 33 together, these proposed experiments will systematically address several key molecular loci of potential damage by mutant huntingtin. Such fundamental mechanistic information is critical to the eventual development of effective therapy for HD. , Ste. 315 San Francisco, Ca 941430962 Timing: Fiscal Year 2006; Project Start 15-JAN-2006; Project End 31-DEC-2009 Summary: (provided by applicant): Polyglutamine neurodegenerative diseases are a devastating family of inherited disorders that include Huntington Disease and spinobulbar muscular atrophy (SBMA).
Transcription factors, including specificity protein 1 (Sp1), have been implicated in HD pathogenesis, but the role of altered Sp1 function in producing mRNA alterations has not been answered. In this application, we take advantage of a well-described set of gene alterations--those occurring in neurotransmitter receptors--as a starting point for determining the molecular mechanisms of transcriptional dysregulation. We propose a series of hypotheses that will yield critical mechanistic insight into the processes that alter mRNA populations and cause disease pathogenesis.
Ds to postdoctoral positions with SNRP scientists at UCC is also presented. • Project Title: SYNAPTIC TOXICITY OF HUNTINGTON DISEASE PROTEIN Principal Investigator & Institution: Li, Xiao-Jiang; Professor; Human Genetics; Emory University 1784 North Decatur Road, Suite 510 Atlanta, Ga 30322 Timing: Fiscal Year 2007; Project Start 01-MAY-2001; Project End 28-FEB-2012 Summary: (provided by applicant): Polyglutamine (polyQ) expansion causes selective neurodegeneration in nine inherited neurological disorders despite the widespread expression of the disease proteins.
Huntington Disease - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers by Philip M. Parker