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| 1 | Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer's disease显示文摘Alzheimer’s disease(AD)is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles.Prior to the development of these characteristic pathological hallmarks of AD,anterograde axonal transport is impaired.However,the key proteins that initiate these intracellular impairments remain elusive.The collapsin response mediator protein-2(CRMP-2)plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2releases kinesin-1.Here,we tested the hypothesis that amyloid-beta(Aβ)-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1(an anterograde axonal motor transport protein)in AD.We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site.Additionally,in the transgenic Tg2576 mouse model of familial AD(FAD)that exhibits Aβaccumulation in the brain with age,we found substantial co-localization of p T555CRMP-2and dystrophic neurites.In SH-SY5Y differentiated neuronal cultures,Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1.The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation.These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function,leading to neuronal defects. | Sara H.Mokhtar Min Joung Kim Kylie A.Magee Pei Mun Aui Speros Thomas Maha M.Bakhuraysah Amani A.Alrehaili Jae Young Lee David L.Steer Rachel Kenny Catriona Mc Lean Michael F.Azari Antonis Birpanagos Ewlina Lipiec Philip Heraud Bayden Wood Steven Petratos | 2018 | Neural Regeneration Research2018，13，6： | 1 |
| 2 | Looking for Cryptosporidium: the applica- tion of advances in detection and diagnosis 显示文摘 | Rachel MC Frank K | 2013 | Int J Parasitol2013，29，5： | 1 |
| 3 | Increased alpha- defensins as a blood marker for schizophrenia susceptibility显示文摘 | Rachel MC Jeffrey TH Edmund Jackson | 2008 | Mol Cell Proteomics2008，7，7： | 1 |
| 4 | Ultrastructure of the denitrifying methanotroph ' Candidatus Methylomirabilis oxyfera,' a novel polygon-shaped bacterium显示文摘 | Wu ML van Teeseling MC Willems M J van Donselaar EG Klingl A Rachel R Geerts WJ Jetten MS Strous M van Niftrik L | | 0，，2： | 1 |
| 5 | A new addition to the cell plan of anammox bacteria:“Candidatus Kuenenia stuttgartiensis” has a protein surface layer as the outermost layer of the cell 显示文摘 | Van Teeseling MC De Almeida NM Klingl A Speth DR Op Den Camp HJ Rachel R Jetten MS Van Niftrik L | 2014 | J Bacteriol2014，196，1： | 1 |
| 6 | From the outside-in: Epidermal targeting as a paradigm for atopic disease therapy显示文摘Atopic dermatitis(AD) is a chronic inflammatory skin disorder which can precede asthma and allergic rhinitis in a disease trajectory known as the atopic march. The pathophysiology of AD includes cutaneous inflammation, disrupted epidermal barrier function, xerosis and propensity to secondary infections. AD had previously been thought to arise from the systemic atopic immune response and therapies are therefore directed towards ameliorating Th2-mediated inflammation. However in recent years the focus has shifted towards primary defects in the skin barrier as an initiating event in AD. Links between loss-of-function variants in the gene encoding filaggrin and disrupted activity of epidermal serine proteases and AD have been reported. Based on these observations, a mechanism has been described by which epidermal barrier dysfunction may lead to inflammation and allergic sensitization. Exogenous and endogenous stressors can further exacerbate inherited barrier abnormalities to promote disease activity. Pathways underlying progression of the atopic march remain unclear, but recent findings implicate thymic stromal lymphopoietin as a factor linking AD to subsequent airway inflammation in asthma. This new appreciation of the epidermis in the development of AD should lead to deployment of more specific strategies to restore barrier function in atopic patients and potentially halt the atopic march. | Rachel MC Gillespie Sara J Brown | 2015 | World Journal of Dermatology2015，4，1： | 0 |
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