Judith A Coppinger's research while affiliated with Royal College of Surgeons in Ireland and other places

... This disease is very common in dogs. So far it has not been reported in the blue fox (Alopex lagopus), while in the grey fox (Urocyon cinereoargenteus) it was not reported until 2016 [Elisen et al. 2004, Gaffney et al. 2014, Gaffney et al. 2016, Rising et al. 2017]. ...

... Platelets can interact with and signal endothelial cells in a variety of ways (6,34,90). In this section we focus on interactions that influence alveolar capillary barrier function because of its central importance in ALI/ARDS, particularly in the early edematous phase (7,30). ...

... Several preclinical and clinical trials of ASA supported its antitumor potential [6,7]. The mechanisms underlying antitumor action of ASA interrelate with its antiinflammatory properties, which are generally result from the inhibition of activity of cyclooxygenases [8,9] along with diminishing platelet activation and thrombosis involved in the cancer progression and metastasis [10,11]. Other reported mechanisms of ASA and its active metabolite SA comprise the inhibition of IkB kinase/NF-kB pathway in vitro and in vivo [12,13], allosteric activation of AMP-activated kinase [14], uncoupling of the respiratory chain by transporting protons across the inner mitochondrial membrane [15]. ...

... In addition, studies revealed unmapped protein-protein interactions of BAG3 with Cells 2020, 9, 2416 3 of 40 proteins such as IFITM-2 (interferon-induced transmembrane protein 2) or STK38 (serine/threonine-protein kinase 38) [69][70][71][72]. Proteomic studies have fundamentally expanded the interactome of BAG3 [33,[72][73][74][75][76][77]. ...

... Given the PIMREG function on proliferation and cell-cycle control 9,10,31,34,35 , together with the ndings presented in this study that PIMREG participates in the DNA damage response with ATM and ATR, it is tempting to speculate that PIMREG may play a role in the ATR-and ATM-dependent checkpoint pathways to block cell cycle progression. ...

... During mitosis, Kif2A localizes to spindle poles where it depolymerizes microtubule minus ends [10,15,16], thereby controlling the rate of poleward microtubule flux. Transport of Kif2A to spindle poles is ensured by minus-end-directed motor protein dynein/dynactin [10] and is increased by interaction with microtubule-associated Dda3 protein, whose expression and phosphorylation are markedly elevated in mitosis [17,18]. Depletion of either Dda3 or Kif2A increases mitotic spindle size [10,17]. ...

... A substantial amount of evidence indicates that hyperactive cofilin forms rods-shape aggregates composed of cofilin and saturated actin filament bundles, known as cofilin/actin rods (Nishida et al., 1987;Minamide et al., 2000Minamide et al., , 2010. Cofilin/actin rods formation in neurons represents a hallmark pathological feature of many neurodegenerative diseases such as Huntington's disease and AD, where it further promotes the progression of the disease (Minamide et al., 2000;Cichon et al., 2012). ...

... α-and dense-granules seem to derive, like lysosomes, from multivesicular precursors [49][50][51]. The content of α-granules consists of a large variety of proteins, such as adhesive molecules (e.g., fibrinogen, VWF, fibronectin, P-selectin), coagulation factors (e.g., FV, FIX, FXIII), anticoagulants (e.g., antithrombin), fibrinolytic proteins (e.g., plasminogen), and growth factors, immune mediators, and integral membrane proteins (e.g., αIIb3, P-selectin) [52,53]. Thus, α-granule proteins can be involved in a large spectrum of physiological functions, such as normal and pathological haemostasis, inflammation, wound healing, antimicrobial response, and cancer metastasis [54,55]. ...

... In postmortem AD brains, Aha1 colocalized with pathogenic tau and correlated with disease progression [90]. In addition to tau, Aha1 stabilizes other Hsp90 clients including mutant cystic fibrosis transmembrane conductance regulator, CFTR, which causes cystic fibrosis [59,100], and mutant melanocortin-4 receptor, another misfolded transmembrane protein [67]. Aha1 may also have a role in RNA processing and DNA repair [96]. ...

... However, the system also has limitations. Whereas chaperone overexpression typically improves the folding capacity of the chaperone system, overexpression of specific chaperones was shown to disrupt folding [19][20][21][22][23] . For example, overexpression of the folding enzyme FKBP51 in a tau transgenic mouse model resulted in accumulation of tau and its toxic oligomers 21 . ...