J
Josée Coulombe
Researcher at Ottawa Hospital Research Institute
Publications - 9
Citations - 151
Josée Coulombe is an academic researcher from Ottawa Hospital Research Institute. The author has contributed to research in topics: Ubiquitin & Proteasome. The author has an hindex of 5, co-authored 9 publications receiving 120 citations.
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Journal ArticleDOI
Evolution of the highly networked deubiquitinating enzymes USP4, USP15, and USP11
Caitlyn Vlasschaert,Caitlyn Vlasschaert,Xuhua Xia,Josée Coulombe,Douglas A. Gray,Douglas A. Gray +5 more
TL;DR: The analyses indicate that USP4 and USP15 arose from whole genome duplication prior to the emergence of jawed vertebrates, and it is confirmed that viability is contingent on a functional copy of USP5 or USP6, while USP11 was generated later in vertebrate evolution by small-scale duplication of the USP 4-encoding region.
Journal ArticleDOI
Loss of UCHL1 promotes age-related degenerative changes in the enteric nervous system
Josée Coulombe,P.P.K.M. Gamage,Madison T. Gray,Mei Zhang,Matthew Y. Tang,John Woulfe,M. Jill Saffrey,Douglas A. Gray,Douglas A. Gray +8 more
TL;DR: The mice displayed functional changes and morphological changes in gut neurons that preceded degenerative changes in the brain, and strongly resemble changes reported for elderly humans, and should serve as a useful model of gut aging.
Journal ArticleDOI
Protection against murine osteoarthritis by inhibition of the 26S proteasome and lysine-48 linked ubiquitination
Marta Radwan,David J. Wilkinson,Wang Hui,Auriane P. M. Destrument,Sarah Charlton,Matt J. Barter,Beth G Gibson,Josée Coulombe,Douglas A. Gray,Andrew D. Rowan,David Young +10 more
TL;DR: The data for the first time identifies a role for ubiquitination and the proteasome in the induction of OA via regulation of inflammatory mediator-induced MMP13 expression and opens avenues of research to determine whether the prote asome, or K48-linked ubiquitinated substrates, are potential therapeutic targets in OA.
Journal ArticleDOI
Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis.
Naomi C. Read,Alex Gutsol,Chet E. Holterman,Anthony Carter,Josée Coulombe,Douglas A. Gray,Chris R. J. Kennedy,Chris R. J. Kennedy,Chris R. J. Kennedy +8 more
TL;DR: The data suggest that UCHL1 upregulation in ACTN4-associated FSGS fuels the proteasome and that UCH l1 deletion may impair proteolysis and thereby preserve K256E/wt-α-actinin-4 heterodimers, maintaining podocyte cytoskeletal integrity and protecting the glomerular filtration barrier.
Journal ArticleDOI
Reversible modulation of SIRT1 activity in a mouse strain.
Katherine V. Clark-Knowles,Xiaohong He,Karen Jardine,Josée Coulombe,Danielle Dewar-Darch,Annabelle Z. Caron,Douglas A. Gray,Douglas A. Gray,Michael W. McBurney,Michael W. McBurney +9 more
TL;DR: This mouse was created to create a mouse in which the SIRT1 activity could be toggled between on and off states by fusing the estrogen receptor ligand-binding domain (ER) to the C terminus of the Sirt1 protein.