Zobrazeno 1 - 10
of 198
pro vyhledávání: '"Ronald, Wetzel"'
Autor:
Ya Zhou, Thomas R. Peskett, Christian Landles, John B. Warner, Kirupa Sathasivam, Edward J. Smith, Shu Chen, Ronald Wetzel, Hilal A. Lashuel, Gillian P. Bates, Helen R. Saibil
Publikováno v:
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-21 (2021)
Abstract Huntington’s disease (HD) is a late onset, inherited neurodegenerative disorder for which early pathogenic events remain poorly understood. Here we show that mutant exon 1 HTT proteins are recruited to a subset of cytoplasmic aggregates in
Externí odkaz:
https://doaj.org/article/0cbf701f6cb54600ae9ad669c9f4899d
Autor:
Kenneth W. Drombosky, Sascha Rode, Ravi Kodali, Tija C. Jacob, Michael J. Palladino, Ronald Wetzel
Publikováno v:
Neurobiology of Disease, Vol 120, Iss , Pp 126-138 (2018)
In Huntington disease (HD), an expanded polyglutamine (polyQ > 37) sequence within huntingtin (htt) exon1 leads to enhanced disease risk. It has proved difficult, however, to determine whether the toxic form generated by polyQ expansion is a misfolde
Externí odkaz:
https://doaj.org/article/9884ce11e91d4fe08225fe51b3471656
Autor:
Hsiang-Kai Lin, Jennifer C. Boatz, Inge E. Krabbendam, Ravindra Kodali, Zhipeng Hou, Ronald Wetzel, Amalia M. Dolga, Michelle A. Poirier, Patrick C. A. van der Wel
Publikováno v:
Nature Communications, Vol 8, Iss 1, Pp 1-12 (2017)
Huntington's disease is caused by a polyglutamine stretch expansion in the first exon of huntingtin. Here, the authors use infrared spectroscopy and solid-state NMR and show that polymorphic huntingtin exon1 fibres differ in their flanking regions bu
Externí odkaz:
https://doaj.org/article/6d1f8de6f3eb481d8704dc203117b49c
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-15 (2016)
The elucidation of amyloid nucleation mechanisms remains challenging as early oligomeric intermediates are transient and difficult to distinguish. Here the authors use Aβ- polyglutamine hybrid peptides designed to slow and limit amyloid maturation t
Externí odkaz:
https://doaj.org/article/db9ce2df521e4e47a3b79fba5fc4d29d
Autor:
Bankanidhi Sahoo, Irene Arduini, Kenneth W Drombosky, Ravindra Kodali, Laurie H Sanders, J Timothy Greenamyre, Ronald Wetzel
Publikováno v:
PLoS ONE, Vol 11, Iss 6, p e0155747 (2016)
Expansion of the polyglutamine (polyQ) track of the Huntingtin (HTT) protein above 36 is associated with a sharply enhanced risk of Huntington's disease (HD). Although there is general agreement that HTT toxicity resides primarily in N-terminal fragm
Externí odkaz:
https://doaj.org/article/0d7d5852f7b5410c952937e6b1b377c6
Autor:
Ronald Wetzel
Publikováno v:
Accounts of Chemical Research. 53:2347-2357
ConspectusHuntington’s disease (HD) is a progressive, familial neurodegenerative disease triggered by the expansion of a polyglutamine (polyQ) track in the protein huntingtin (htt). PolyQ sequences...
Autor:
Kirupa Sathasivam, Helen R. Saibil, Christian Landles, Ronald Wetzel, Ya Zhou, Hilal A. Lashuel, Shu Chen, Edward J Smith, Thomas R. Peskett, Gillian P. Bates, John B. Warner
Huntington’s disease (HD) is a late onset, inherited neurodegenerative disorder for which early pathogenic events remain poorly understood. Here we show that mutant exon 1 HTT proteins are recruited to a subset of cytoplasmic aggregates in the cell
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::544a420c8f2fa9b3ec5f04e71ecbe9da
https://doi.org/10.1101/2021.03.05.433899
https://doi.org/10.1101/2021.03.05.433899
Autor:
Thomas R. Peskett, John B. Warner, Hilal A. Lashuel, Shu Chen, Ya Zhou, Gillian P. Bates, Ronald Wetzel, Kirupa Sathasivam, Edward J Smith, Helen R. Saibil, Christian Landles
Publikováno v:
Acta Neuropathologica Communications
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-21 (2021)
Acta Neuropathologica Communications, 9 (1)
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-21 (2021)
Acta Neuropathologica Communications, 9 (1)
Huntington’s disease (HD) is a late onset, inherited neurodegenerative disorder for which early pathogenic events remain poorly understood. Here we show that mutant exon 1 HTT proteins are recruited to a subset of cytoplasmic aggregates in the cell
Autor:
Sascha Rode, Ronald Wetzel, Michael J. Palladino, Ravi Kodali, Kenneth W. Drombosky, Tija C. Jacob
Publikováno v:
Neurobiology of Disease, Vol 120, Iss, Pp 126-138 (2018)
In Huntington disease (HD), an expanded polyglutamine (polyQ > 37) sequence within huntingtin (htt) exon1 leads to enhanced disease risk. It has proved difficult, however, to determine whether the toxic form generated by polyQ expansion is a misfolde
Autor:
Amantha Thathiah, J. Timothy Greenamyre, Yaqun Teng, Ravindra Kodali, Weixing Zhao, Maria E. Rubio, Ronald Wetzel, Arthur S. Levine, Starr Welty, Zhuobin Liang, Laurie H. Sanders, Li Lan
Publikováno v:
Journal of Biological Chemistry. 293:1353-1362
It has been long assumed that post-mitotic neurons only utilize the error-prone non-homologous end–joining pathway to repair double-strand breaks (DSBs) associated with oxidative damage to DNA, given the inability of non-replicating neuronal DNA to