Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Ian R Kelsall"'
Publikováno v:
PLoS ONE, Vol 7, Iss 5, p e36970 (2012)
The many proteins that function in the Fanconi anaemia (FA) monoubiquitylation pathway initiate replicative DNA crosslink repair. However, it is not clear whether individual FA genes participate in DNA repair pathways other than homologous recombinat
Externí odkaz:
https://doaj.org/article/591308a5da0d441b86b6059e5a89f409
Autor:
Ian R. Kelsall
Publikováno v:
Frontiers in Molecular Biosciences, Vol 9 (2022)
The post-translational modification of proteins with ubiquitin plays a central role in nearly all aspects of eukaryotic biology. Historically, studies have focused on the conjugation of ubiquitin to lysine residues in substrates, but it is now clear
Externí odkaz:
https://doaj.org/article/da0b4c7a458c48ada15ec53fcf7849de
Autor:
Ian R Kelsall, Elisha H McCrory, Yingqi Xu, Cheryl L Scudamore, Sambit K Nanda, Paula Mancebo‐Gamella, Nicola T Wood, Axel Knebel, Stephen J Matthews, Philip Cohen
Publikováno v:
The EMBO journal. 41(8)
HOIL-1, a component of the linear ubiquitin chain assembly complex (LUBAC), ubiquitylates serine and threonine residues in proteins by esterification. Here, we report that mice expressing an E3 ligase-inactive HOIL-1[C458S] mutant accumulate polygluc
Autor:
Philip Cohen, Nicola T. Wood, Sambit K. Nanda, Ian R. Kelsall, Elisha H. McCrory, Paula Mancebo-Gamella, Stephen Matthews, Yingqi Xu, Axel Knebel, Cheryl L. Scudamore
HOIL-1, a component of the Linear Ubiquitin Assembly Complex (LUBAC), ubiquitylates serine and threonine residues in proteins, forming ester bonds (Kelsall et al, 2019, PNAS 116, 13293-13298). Here we report that mice expressing the E3 ligase-inactiv
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::bca3b0236fb1def26f7875b0dac08f40
https://doi.org/10.1101/2021.09.10.459791
https://doi.org/10.1101/2021.09.10.459791
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America
Significance The formation of isopeptide bonds between the C-terminal carboxylate of ubiquitin and ε-amino groups of lysine residues on another protein is a major mechanism for regulating protein function. Ubiquitin can also form peptide bonds with
Publikováno v:
Advances in Biological Regulation
Components of bacteria and viruses activate Toll-Like Receptors in host cells, triggering the formation of the Myddosome and a signalling network that culminates in the production and release of the inflammatory mediators required to combat pathogeni
Autor:
Ian R. Kelsall, Arno F. Alpi, Nicola T. Wood, Yosua Adi Kristariyanto, Axel Knebel, Yogesh Kulathu
Publikováno v:
The Journal of Biological Chemistry
Journal of Biological Chemistry
Journal of Biological Chemistry
Cullin-RING E3 ubiquitin ligases (CRLs) are large and diverse multisubunit protein complexes that contribute to about one-fifth of ubiquitin-dependent protein turnover in cells. CRLs are activated by the attachment of the ubiquitin-like protein neura
Autor:
Ian R. Kelsall, Thomas Macartney, Mark Peggie, Eddy T. H. Goh, Jiazhen Zhang, Christoph H. Emmerich, J. Simon C. Arthur, Philip Cohen, Sam Strickson, C. James Hastie, Francesco Marchesi, Axel Knebel
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America. 114(17)
It is widely accepted that the essential role of TRAF6 in vivo is to generate the Lys63-linked ubiquitin (K63-Ub) chains needed to activate the “master” protein kinase TAK1. Here, we report that TRAF6 E3 ligase activity contributes to but is not
Publikováno v:
Journal of Neurochemistry. 118:596-610
J. Neurochem. (2011) 118, 596–610. Abstract Abnormal regulation of brain glycogen metabolism is believed to underlie insulin-induced hypoglycaemia, which may be serious or fatal in diabetic patients on insulin therapy. A key regulator of glycogen l
Autor:
Patricia T.W. Cohen, Martin Voss, Ian R. Kelsall, James Paterson, C. James Hastie, Cristina Martin-Granados, Mark Peggie
Publikováno v:
Cellular Signalling. 23:114-124
Activation of 5'-AMP-activated protein kinase (AMPK) is believed to be the mechanism by which the pharmaceuticals, metformin and phenformin, exert their beneficial effects for treatment of type 2 diabetes. These biguanide drugs elevate 5'-AMP, which