Zobrazeno 1 - 10
of 11
pro vyhledávání: '"John S. Bett"'
Autor:
John S Bett, Naheed Kanuga, Emma Richet, Gunter Schmidtke, Marcus Groettrup, Michael E Cheetham, Jacqueline van der Spuy
Publikováno v:
PLoS ONE, Vol 7, Iss 2, p e30866 (2012)
Mutations in AIPL1 cause the inherited blindness Leber congenital amaurosis (LCA). AIPL1 has previously been shown to interact with NUB1, which facilitates the proteasomal degradation of proteins modified with the ubiquitin-like protein FAT10. Here w
Externí odkaz:
https://doaj.org/article/1a4f9d7feff04e6d8faa780b2f448247
Publikováno v:
PLoS ONE, Vol 4, Iss 4, p e5128 (2009)
Impairment of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the selective dysfunction and death of neurons in polyglutamine disorders such as Huntington's disease (HD). The fact that inclusion bodi
Externí odkaz:
https://doaj.org/article/5e7d484c2c604e6c933cf709e64ec349
Autor:
John S. Bett
Publikováno v:
Essays in Biochemistry. 60:143-151
Cells have developed an evolutionary obligation to survey and maintain proteome fidelity and avoid the possible toxic consequences of protein misfolding and aggregation. Disturbances to protein homoeostasis (proteostasis) can result in severe cellula
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d9c5af3ae86c8acb9ca3a4ed84c5157b
https://doi.org/10.1042/ebc20160001
https://doi.org/10.1042/ebc20160001
Publikováno v:
Journal of Cellular and Molecular Medicine
Huntington's disease (HD) is an inherited neurodegenerative disease caused by the expansion of a polyglutamine tract in the protein huntingtin (htt). HD brains are characterized by the presence of ubiquitin‐positive neuronal inclusion bodies, sugge
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b228f6acc17141a60d42e661a54ea947
http://europepmc.org/articles/PMC2892477
http://europepmc.org/articles/PMC2892477
Publikováno v:
Progress in Retinal and Eye Research
Molecular chaperones facilitate and regulate protein conformational change within cells. This encompasses many fundamental cellular processes: including the correct folding of nascent chains; protein transport and translocation; signal transduction a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ae14b5b3e67cf1657ccae675c797128c
https://doi.org/10.1016/j.preteyeres.2008.03.001
https://doi.org/10.1016/j.preteyeres.2008.03.001
Publikováno v:
Journal of Visualized Experiments.
Post-translational modification of proteins with ubiquitin and ubiquitin-like molecules (UBLs) is emerging as a dynamic cellular signaling network that regulates diverse biological pathways including the hypoxia response, proteostasis, the DNA damage
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6806fc32e46f45dd051151c688c3f8bf
https://doi.org/10.3791/51572-v
https://doi.org/10.3791/51572-v
Autor:
Ronald T. Hay, Patrick G. A. Pedrioli, Adel F. M. Ibrahim, John S. Bett, Amit K. Garg, Sonia Rocha, Van Kelly
Publikováno v:
Biochemical Journal
HIF1A (hypoxia-inducible factor 1α) is the master regulator of the cellular response to hypoxia and is implicated in cancer progression. Whereas the regulation of HIF1A protein in response to oxygen is well characterized, less is known about the fat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ffe9595871df7ee3d6e3a8d7fdf77458
https://pubmed.ncbi.nlm.nih.gov/23398456
https://pubmed.ncbi.nlm.nih.gov/23398456
Autor:
Gunter Schmidtke, Michael E. Cheetham, Marcus Groettrup, John S. Bett, Emma Richet, Naheed Kanuga, Jacqueline van der Spuy
Publikováno v:
PLoS ONE
PLoS ONE, Vol 7, Iss 2, p e30866 (2012)
PLoS ONE, Vol 7, Iss 2, p e30866 (2012)
Mutations in AIPL1 cause the inherited blindness Leber congenital amaurosis (LCA). AIPL1 has previously been shown to interact with NUB1, which facilitates the proteasomal degradation of proteins modified with the ubiquitin-like protein FAT10. Here w
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::75850936297b44a5574cc94a461d7681
https://pubmed.ncbi.nlm.nih.gov/22347407
https://pubmed.ncbi.nlm.nih.gov/22347407
Publikováno v:
PLoS ONE, Vol 4, Iss 4, p e5128 (2009)
PLoS ONE
PLoS ONE
Impairment of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the selective dysfunction and death of neurons in polyglutamine disorders such as Huntington's disease (HD). The fact that inclusion bodi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1f15d6efd96296ed4379daa38778b2c0
https://eprints.gla.ac.uk/102884/1/102884.pdf
https://eprints.gla.ac.uk/102884/1/102884.pdf
This chapter discusses molecular pathogenesis and therapeutic targets in Huntington's disease (HD). HD is an autosomal dominant, late onset neurodegenerative disease that is caused by a CAG/polyglutamine repeat expansion. Individuals with HD usually
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9e22313339f610a12493d3d90ee15f4d
https://doi.org/10.1016/b978-012369462-1/50015-6
https://doi.org/10.1016/b978-012369462-1/50015-6