The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.

By J. Steffan, A. Kazantsev, O. Spasic-Boskovic, Marilee Greenwald, Ya-zhen Zhu, H. Göhler, Erich E. Wanker, G. Bates, D. Housman, Leslie M. Thompson. Proceedings of the National Academy of Sciences of the United States of America, 2000

1,101 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/11230751a514354bbdd94148e5c2119bfa9d1f17

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. E. Cattaneo
2. C. Zuccato
3. M. Valenza

In Molecular Biology

1. E. Cattaneo
2. Leslie M. Thompson
3. M. Valenza
4. J. Tyedmers
5. C. Zuccato
6. Axel Mogk
7. Bernd Bukau

Citations in the corpus

• Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines (2002, background): “, perhaps through its interactions with CREB (cAMP response element binding protein”
• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “Moreover, mutant huntingtin can interact Physiol Rev • VOL 90 • JULY 2010 • www.prv.org by 10.220.33.4 on O ctober 9, 2016 http://physrev.physiology.org/ D ow nloaded from with both the glutamine-rich activation domain and the acetyltransferase domain of CBP, causing a reduction in histone acetylati”
• Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila (2001, background): “We previously found that a fragment of mutant Htt interacts directly with CBP, which contains an acetyltransferase domain and is a co-activator of numerous promoter”
• Cellular strategies for controlling protein aggregation (2010, background): “This trapping of other proteins in aggregates was suggested to be one possible reason for the toxicity associated with neurodegenerative diseases that involves polyglutamine aggregatio”
• Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice (2003, positive): “Mutant huntingtin can bind to histone acetyltransferase domains and reduce this activity, resulting in a reduction in histone acetylation and in repressed gene transcription (Steffan et al., 2000).”