| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Clara R L Teo, Wen Wang, Hai Yang Law, Caroline G Lee, Samuel S Chon. Single-step scalable-throughput molecular screening for Huntington disease. Clinical chemistry. vol 54. issue 6. 2008-07-02. PMID:18403567. |
huntington disease (hd) is a fatal autosomal dominant neurodegenerative disorder caused by an unstable expansion of the cag trinucleotide repeat in exon 1 of the htt (huntingtin) gene and typically has an adult onset. |
2008-07-02 |
2023-08-12 |
Not clear |
| Pritha Majumder, Swasti Raychaudhuri, Biswanath Chattopadhyay, Nitai P Bhattacharyy. Increased caspase-2, calpain activations and decreased mitochondrial complex II activity in cells expressing exogenous huntingtin exon 1 containing CAG repeat in the pathogenic range. Cellular and molecular neurobiology. vol 27. issue 8. 2008-05-01. PMID:17902043. |
(1) huntington's disease (hd) is an autosomal dominant neurodegenerative disease caused by the expansion of polymorphic cag repeats beyond 36 at exon 1 of huntingtin gene (htt). |
2008-05-01 |
2023-08-12 |
Not clear |
| V Perez-De La Cruz, A Santamari. Integrative hypothesis for Huntington's disease: a brief review of experimental evidence. Physiological research. vol 56. issue 5. 2008-02-14. PMID:17184144. |
neurochemical changes are specifically oriented to deplete gabaergic and cholinergic systems, while molecular alterations include an increased expression of cag trinucleotide at exon 1 from the huntingtin (htt) gene, as well as aggregation of mutant htt. |
2008-02-14 |
2023-08-12 |
mouse |
| Justin R Prigge, Edward E Schmid. HAP1 can sequester a subset of TBP in cytoplasmic inclusions via specific interaction with the conserved TBP(CORE). BMC molecular biology. vol 8. 2007-12-27. PMID:17868456. |
huntington's disease, spinal and bulbar muscular atrophy, and spinocerebellar ataxia 17 (sca17) are caused by expansions in the polyglutamine (polyq) repeats in huntingtin protein (htt), androgen receptor protein (ar), and tata-binding protein (tbp), respectively. |
2007-12-27 |
2023-08-12 |
Not clear |
| Erica Scappini, Tong-Wey Koh, Negin P Martin, John P O'Brya. Intersectin enhances huntingtin aggregation and neurodegeneration through activation of c-Jun-NH2-terminal kinase. Human molecular genetics. vol 16. issue 15. 2007-12-18. PMID:17550941. |
huntingon's disease is a progressive neurodegenerative disease arising from expansion of a polyglutamine (polyq) tract in the protein huntingtin (htt) resulting in aggregation of mutant htt into nuclear and/or cytosolic inclusions in neurons. |
2007-12-18 |
2023-08-12 |
drosophila_melanogaster |
| Ming-Chang Chiang, Chiun-Gung Juo, Hao-Hung Chang, Hui-Mei Chen, Eugene C Yi, Yijuang Cher. Systematic uncovering of multiple pathways underlying the pathology of Huntington disease by an acid-cleavable isotope-coded affinity tag approach. Molecular & cellular proteomics : MCP. vol 6. issue 5. 2007-12-12. PMID:17272267. |
huntington disease (hd) is an autosomal dominant neurodegenerative disease that results from a cag (glutamine) trinucleotide expansion in exon 1 of huntingtin (htt). |
2007-12-12 |
2023-08-12 |
mouse |
| Kyung-Jin Lee, Antony Panzera, David Rogawski, Lois E Greene, Evan Eisenber. Cellular prion protein (PrPC) protects neuronal cells from the effect of huntingtin aggregation. Journal of cell science. vol 120. issue Pt 15. 2007-12-06. PMID:17635996. |
the effect of normal cellular prion protein (prp(c)) on abnormal protein aggregation was examined by transfecting huntingtin fragments (htt) into sn56 neuronal-derived cells depleted of prp(c) by rna interference. |
2007-12-06 |
2023-08-12 |
mouse |
| Hirokazu Fukui, Carlos T Morae. Extended polyglutamine repeats trigger a feedback loop involving the mitochondrial complex III, the proteasome and huntingtin aggregates. Human molecular genetics. vol 16. issue 7. 2007-08-28. PMID:17356014. |
mitochondrial abnormalities represent a major cytopathology in huntington's disease (hd), a fatal neurodegenerative disease caused by cag repeat expansions in the gene encoding huntingtin (htt). |
2007-08-28 |
2023-08-12 |
human |
| Shihua Li, Xiao-Jiang L. Multiple pathways contribute to the pathogenesis of Huntington disease. Molecular neurodegeneration. vol 1. 2007-07-20. PMID:17173700. |
huntington disease (hd) is caused by expansion of a polyglutamine (polyq) domain in the protein known as huntingtin (htt), and the disease is characterized by selective neurodegeneration. |
2007-07-20 |
2023-08-12 |
Not clear |
| Ming-Chang Chiang, Hui-Mei Chen, Yi-Hsin Lee, Hao-Hung Chang, Yi-Chih Wu, Bing-Wen Soong, Chiung-Mei Chen, Yih-Ru Wu, Chin-San Liu, Dau-Ming Niu, Jer-Yuarn Wu, Yuan-Tsong Chen, Yijuang Cher. Dysregulation of C/EBPalpha by mutant Huntingtin causes the urea cycle deficiency in Huntington's disease. Human molecular genetics. vol 16. issue 5. 2007-07-16. PMID:17213233. |
huntington's disease (hd) is an autosomal dominant neurodegenerative disease caused by a cag trinucleotide expansion in the huntingtin (htt) gene. |
2007-07-16 |
2023-08-12 |
mouse |
| Bin Huang, Johannes Schiefer, Christian Sass, G Bernhard Landwehrmeyer, Christoph M Kosinski, Stefan Kochane. High-capacity adenoviral vector-mediated reduction of huntingtin aggregate load in vitro and in vivo. Human gene therapy. vol 18. issue 4. 2007-06-19. PMID:17472569. |
huntington's disease (hd) is an autosomal dominant neurodegenerative disease caused by the expansion of a cag trinucleotide repeat in exon 1 of the huntingtin (htt) gene. |
2007-06-19 |
2023-08-12 |
mouse |
| Gabriele Schilling, Alexandra Klevytska, Andrew T N Tebbenkamp, Katrin Juenemann, Jillian Cooper, Victoria Gonzales, Hilda Slunt, Michelle Poirer, Christopher A Ross, David R Borchel. Characterization of huntingtin pathologic fragments in human Huntington disease, transgenic mice, and cell models. Journal of neuropathology and experimental neurology. vol 66. issue 4. 2007-05-15. PMID:17413322. |
huntington disease (hd) is caused by the expansion of a glutamine (q) repeat near the n terminus of huntingtin (htt), resulting in altered conformation of the mutant protein to produce, most prominently in brain neurons, nuclear and cytoplasmic inclusion pathology. |
2007-05-15 |
2023-08-12 |
mouse |
| Stephanie L H Miller, Erica L Scappini, John O'Brya. Ubiquitin-interacting motifs inhibit aggregation of polyQ-expanded huntingtin. The Journal of biological chemistry. vol 282. issue 13. 2007-05-10. PMID:17276991. |
given the presence of these ubiquitin-binding proteins in the insoluble aggregates, we examined whether heterologous expression of short motifs that bind ubiquitin, termed ubiquitin-interacting motifs (uims), altered the aggregation of polyq-expanded huntingtin (htt), the protein product of the huntington disease gene. |
2007-05-10 |
2023-08-12 |
Not clear |
| Paul R Dahlgren, Mikhail A Karymov, John Bankston, Tina Holden, Peter Thumfort, Vernon M Ingram, Yuri L Lyubchenk. Atomic force microscopy analysis of the Huntington protein nanofibril formation. Nanomedicine : nanotechnology, biology, and medicine. vol 1. issue 1. 2007-03-05. PMID:17292058. |
huntington's disease is an autosomal dominant progressive neurodegenerative disease associated with dramatic expansion of a polyglutamine sequence in exon 1 of the huntingtin protein htt that leads to cytoplasmic, and even nuclear aggregation of fibrils. |
2007-03-05 |
2023-08-12 |
Not clear |
| Dianne S Schwarz, Hongliu Ding, Lori Kennington, Jessica T Moore, Janell Schelter, Julja Burchard, Peter S Linsley, Neil Aronin, Zuoshang Xu, Phillip D Zamor. Designing siRNA that distinguish between genes that differ by a single nucleotide. PLoS genetics. vol 2. issue 9. 2007-01-29. PMID:16965178. |
we systematically identified sirnas that discriminate between the wild-type and mutant alleles of two disease genes: the human cu, zn superoxide dismutase (sod1) gene, which contributes to the progression of hereditary amyotrophic lateral sclerosis through the gain of a toxic property, and the huntingtin (htt) gene, which causes huntington disease when its cag-repeat region expands beyond approximately 35 repeats. |
2007-01-29 |
2023-08-12 |
human |
| Jeremy M Van Raamsdonk, Jacqueline Pearson, Zoe Murphy, Michael R Hayden, Blair R Leavit. Wild-type huntingtin ameliorates striatal neuronal atrophy but does not prevent other abnormalities in the YAC128 mouse model of Huntington disease. BMC neuroscience. vol 7. 2007-01-23. PMID:17147801. |
huntington disease (hd) is an adult onset neurodegenerative disorder caused by a polyglutamine expansion in the huntingtin (htt) protein. |
2007-01-23 |
2023-08-12 |
mouse |
| Jonathan Cornett, Lauren Smith, Meyer Friedman, Ji-Yeon Shin, Xiao-Jiang Li, Shi-Hua L. Context-dependent dysregulation of transcription by mutant huntingtin. The Journal of biological chemistry. vol 281. issue 47. 2007-01-09. PMID:17012230. |
huntington disease (hd) is an adult-onset neurodegenerative disease caused by expansion of a polyglutamine (poly(q) tract in the n-terminal region of huntingtin (htt). |
2007-01-09 |
2023-08-12 |
Not clear |
| Wei Li, Louise C Serpell, Wendy J Carter, David C Rubinsztein, James A Huntingto. Expression and characterization of full-length human huntingtin, an elongated HEAT repeat protein. The Journal of biological chemistry. vol 281. issue 23. 2006-08-23. PMID:16595690. |
huntington disease is an inherited neurodegenerative disorder that is caused by expanded cag trinucleotide repeats, resulting in a polyglutamine stretch of >37 on the n terminus of the protein huntingtin (htt). |
2006-08-23 |
2023-08-12 |
mouse |
| Jeremy M Van Raamsdonk, William T Gibson, Jacqueline Pearson, Zoe Murphy, Ge Lu, Blair R Leavitt, Michael R Hayde. Body weight is modulated by levels of full-length huntingtin. Human molecular genetics. vol 15. issue 9. 2006-08-16. PMID:16571604. |
huntington disease is an adult-onset neurodegenerative disorder that is caused by the expansion of a polyglutamine tract within the huntingtin (htt) protein. |
2006-08-16 |
2023-08-12 |
mouse |
| Zhihua Qiu, Fran Norflus, Bhupinder Singh, Mary K Swindell, Rodica Buzescu, Michelle Bejarano, Raman Chopra, Birgit Zucker, Caroline L Benn, Derek P DiRocco, Jang-Ho J Cha, Robert J Ferrante, Steven M Hersc. Sp1 is up-regulated in cellular and transgenic models of Huntington disease, and its reduction is neuroprotective. The Journal of biological chemistry. vol 281. issue 24. 2006-08-01. PMID:16595660. |
interactions between mutant huntingtin (htt) and a variety of transcription factors including specificity proteins (sp) have been suggested as a central mechanism in huntington disease (hd). |
2006-08-01 |
2023-08-12 |
mouse |