Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity

By F. Nucifora, M. Sasaki, M. F. Peters, H. Huang, J. Cooper, M. Yamada, H. Takahashi, S. Tsuji, J. Troncoso, Valina L. Dawson and 2 more. Science, 2001

1,143 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/bae2ac4bdd56380d66cc5b09b7c9876acc417996

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Citations in the corpus

Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration. (2004, background): “…histones and the extenhas been associated with a reduction in CBP activitysion of these analyses to other mouse mutants in HAT (McCampbell et al., 2000; Nucifora et al., 2001), FADand HDAC genes should aid in the analysis of the hismutations may cause a gain of transcriptional functiontone code.”
Natively unstructured regions in proteins identified from contact predictions (2007, background): “The aggregation of proteins with unstructured regions has also been associated with neurodegenerative diseases, e.g., Huntington's disease is directly linked to the aggregation of polyglutamine from CBP (Nucifora, et al., 2001).”
ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats. (2002, background): “Genetic and molecular studies suggest that polyQ causes alteration of gene expression, abnormal protein interactions, alteration of proteolysis, and activation of caspases and protein unfolding (Paulson et al. 2000; McCampbell and Fischbeck 2001; Nucifora et al. 2001).”
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”
Variable tandem repeats accelerate evolution of coding and regulatory sequences. (2010, background): “The expanded polyglutamine tract interferes with the interaction of htt and its numerous partners in the nucleus, such as the global transcriptional activator CREB binding protein (CBP), resulting in aberrant expression of target genes (91).”
Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. (2004, background): “…found a selective reductionleading to reduced CRE-dependent gene expression, has been implicated in the pathogenesis of neurodegen- in NMDA receptor-mediated responses and synaptic levels of NMDA receptors and CaMKII in mutant mice.eration in polyglutamine repeat disorders (Nucifora et al., 2001).”