Sp1 and TAFII130 Transcriptional Activity Disrupted in Early Huntington's Disease
By A. Dunah, Hyunkyung Jeong, A. Griffin, Yong-Man Kim, D. Standaert, S. Hersch, M. Mouradian, A. Young, N. Tanese, D. Krainc. Science, 2002
715 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/8c8f79e5af9d6ef3cce6378bdc94f8d7ad7bb350
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In Cellular and Molecular Neuroscience
In Molecular Biology
Citations in the corpus
- Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “TFIID, TFIIF, and TAFII130, which are components of the core transcriptional machinery, are direct targets of mutant huntingtin (162, 523, 659).”
- Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice (2003, neutral): “Nonspecific binding was inhibited by incubation in Tris-buffered saline–Tween 20 (TBST) (50 mM Tris HCl, pH 8.0, 0.9% NaCl, 0.1% Tween 20) containing 5% nonfat dry milk for 0.5 hr. Primary antibodies against Sp1 (PEP2; Santa Cruz Biotechnology, Santa Cruz, CA) were diluted at 1:1000 in 1% milk TBST ”
- Hydrogen peroxide sensing, signaling and regulation of transcription factors (2014, background): “SP1 directly interacts with TATA-binding protein associated factors [123] and other factors, such as those binding to cAMP response elements [124], NF-B [125] and vascular endothelial growth factor receptor-2 (VEGFR-2) [126].”