期刊
PROGRESS IN NEUROBIOLOGY
卷 83, 期 4, 页码 249-259出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2007.02.005
关键词
Huntington's disease; transcriptional dysregulation; mutant huntingtin; transcription factor(s); small molecule; neuroprotection
资金
- NCCIH NIH HHS [U01 AT000613-06A1, R01 AT000613, AT00613, U01 AT000613] Funding Source: Medline
- NINDS NIH HHS [NS35255, R01 NS035255-06, P01 NS045242, NS045242, P01 NS045242-05] Funding Source: Medline
Transcriptional dysregulation in Huntington's disease (HD) is a well documented and broadly studied phenomenon. Its basis appears to be in huntingtin's aberrant protein-protein interactions with a variety of transcription factors. The development of therapeutics targeting altered transcription, however, faces serious challenges. No single transcriptional regulator has emerged as a primary actor in HD. The levels of literally hundreds of RNA transcripts are altered in affected cells and it is uncertain which are most relevant. The protein-protein interactions of mutant huntingtin with transcriptional factors do not constitute conventional and easy targets for drug molecules. Nevertheless, potential therapeutic advances, targeting transcriptional deregulation in HD, have been made in recent years. In this chapter we review current progress in this area of therapeutic development. We also discuss possible drug discovery strategies targeting altered transcriptional pathways. (C) 2007 Elsevier Ltd. All rights reserved.
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