The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Dominant phenotypes produced by the HD mutation in STHdhQ111 striatal cells
Open accessAbstract
Lengthening a glutamine tract in huntingtin confers a dominant attribute that initiates degeneration of striatal neurons in Huntington's disease (HD). To identify pathways that are candidates for the mutant protein's abnormal function, we compared striatal cell lines established from wild-type and Hdh(Q111) knock-in embryos. Alternate versions of full-length huntingtin, distinguished by epitope accessibility, were localized to different sets of nuclear and perinuclear organelles involved in RNA biogenesis and membrane trafficking. However, mutant STHdh(Q111) cells also exhibited additional forms of the full-length mutant protein and displayed dominant phenotypes that did not mirror phenotypes caused by either huntingtin deficiency or excess. These phenotypes indicate a disruption of striatal cell homeostasis by the mutant protein, via a mechanism that is separate from its normal activity. They also support specific stress pathways, including elevated p53, endoplasmic reticulum stress response and hypoxia, as potential players in HD.
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MACDONALD, M. (1993) · Cell · doi:10.1016/0092-8674(93)90585-e · Cited by 8,366
Scherzinger, E., Lurz, R., Turmaine, M., Mangiarini, L., Hollenbach, B., Hasenbank, R., Bates, G. P., Davies, S. W., Lehrach, H., & Wanker, E. E. (1997) · Cell · doi:10.1016/s0092-8674(00)80514-0 · Cited by 1,291 · cited 1×
“The specific huntingtin reagents were as follows: EM48 (amino acids 1–256) (45), AP194 (amino acids 1–17), AP229 (amino acids 55–66), HP1 (amino acids 80–113), HF1 (amino acids 1981–2580) (14,23), mAb 2166 (amino acids 181–810) (Chemicon International, Temecula, CA) and mAb 1F8 (3,35).”
Mice without telomerase: what can they teach us about human cancer?
Artandi, S. E., & DePinho, R. A. (2000) · Nature Medicine · doi:10.1038/78595 · Cited by 126
Cited by
Gauthier, L. R., Charrin, B. C., Borrell-Pagès, M., Dompierre, J. P., Rangone, H., Cordelières, F. P., De Mey, J., MacDonald, M. E., Leßmann, V., Humbert, S., et al. (2004) · Cell · doi:10.1016/j.cell.2004.06.018 · Cited by 1,178
Loss of Huntingtin-Mediated BDNF Gene Transcription in Huntington's Disease
Zuccato, C., Ciammola, A., Rigamonti, D., Leavitt, B. R., Goffredo, D., Conti, L., MacDonald, M. E., Friedlander, R. M., Silani, V., Hayden, M. R., et al. (2001) · Science · doi:10.1126/science.1059581 · Cited by 1,123
Cannabidiol is a negative allosteric modulator of the cannabinoid CB 1 receptor
Laprairie, R. B., Bagher, A. M., Kelly, M. E. M., & Denovan‐Wright, E. M. (2015) · British Journal of Pharmacology · doi:10.1111/bph.13250 · Cited by 1,039
Cui, L., Jeong, H., Borovecki, F., Parkhurst, C. N., Tanese, N., & Krainc, D. (2006) · Cell · doi:10.1016/j.cell.2006.09.015 · Cited by 1,012
Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes
Zuccato, C., Tartari, M., Crotti, A., Goffredo, D., Valenza, M., Conti, L., Cataudella, T., Leavitt, B. R., Hayden, M. R., Timmusk, T., et al. (2003) · Nature Genetics · doi:10.1038/ng1219 · Cited by 979
Metadata
- Authors
- Trettel, F.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-11-01
- Volume
- 9
- Issue
- 19
- Pages
- 2799-2809
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2135783352
- Cited by
- 610
- References
- 3
- FWCI
- 3.31
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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