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17篇 您的检索式:作者名="Maud B"
    题名 作者 年代 出处 被引量
1Maize HapMap2 identifies extant variation from a genome in flux 显示文摘Jer-Ming Chia Chi Song Peter J Bradbury Denise Cos- tich Natalia de Leon John Doebley Robert J Elshire Brandon Gaut Laura Geller Jeffrey C Glaubitz Michael Gore Kate E Guill Jim Holland Matthew B Hufford Jinsheng Lai Meng Li Xin Liu Yanli Lu Richard Mc- Combie Rebecca Nelson Jesse Poland Boddupalli M Prasanna Tanja Pyhajarvi Tingzhao Rong Rajandeep S Sekhon Qi Sun Maud I Tenaillon Feng Tian Jun Wang Xun Xu Zhiwu Zhang Shawn M Kaeppler Jef- frey Ross-lbarra Michael D McMullen Edward S Buck- ler Gengyun Zhang Yunbi Xu Doreen Ware 2012Nat Genet2012,,44:1
2Starvation survival of the stored product pest Liposcelis bostrychophilus Badonnel (Psocoptera, Liposcelidae) 显示文摘Turner B D Maude - Roxby H 1988Journal of Stored Product Research1988,24,1:1
3Crosstalk between the canonical NF-[kappa]B and Notch signaling pathways inhibits Ppar[gamma] expression and promotes pancreatic cancer progression in mice显示文摘Maniati Eleni Bossard Maud Cook Natalie Candido Juliana B Emami-Shahri Nia Nedospasov Sergei A Balkwill Frances R Tuveson David A Hagemann Thorsten 2011Journal of Clinical Investigation2011,,12:1
4Treatments to control Phoma and Alternafia infections of brassica seeds显示文摘Maude R B F M Humpherson-Jones C G Shuring 1984Plant Pathology1984,33,:1
5From GCM grid cell to agricultural plot scale issues affecting modeling of climate impact显示文摘CHRISTIAN B BENJAMIN S MAUD B 2005Phibs T Roy Soc B2005,360,:1
6Biomaterial-associated thrombosis: roles of coagulation factors, complement, platelets and leukocytes 显示文摘MAUD B GORBET M SEFTON M V 2004Biomaterials2004,25,:1
7Studies on the epidemiology of Alternaria brassicicola in Brassica oleracea seed production crops显示文摘Humpherson-Jones F M Maude R B 1982Annals of Applied Biology1982,100,:1
8种子处理显示文摘在传统上,人们一直采用种子处理来消灭种传病害并使种子和幼苗免遭土传病害和害虫的为害。然而,现在种子处理这个术语包含着更为广泛的内容,除病理学问题外,它可用于改变种子的生理学特性,从而改进种子的物理性能。而且,人们还发明了新的施用技术,使农药、生物药剂等得以非常准确地施于种子。因此。R B Maude 雷得漾 1992农药译丛1992,14,6:1
9Elaboration of monodisperse spherical hollow particles with ordered mesoporous silica shells via dual latex/surfactant templating: radial orientation of mesopore channels显示文摘Helene B Maud S Pasetto P 2008Langmuir2008,24,13:1
10查看详情显示文摘K L Lee B Grémaud R Han B G Euglert and C Miniatura 0,,04:1
11Relationship between compressive strength and cervical shaping of the all ceramic cerestore crown显示文摘 Maud B 1987Swed Dent J1987,11,:1
12查看详情显示文摘D Poletti C Miniatura B Grémaud 0,,03:1
13Studies on the seed-borne phases of dark leaf spot (Alternar- ia brassicicola ) and grey leaf spot (Alternaria brassi- cae) of brassicas 显示文摘MAUDE R B HUMPHERSON-JONES F M 1980Annals of Applied Biology1980,95,3:1
14Pressure stability with CPAP devices:a bench evaluation显示文摘Bruno L Karl Maud B 2010Sleep Medicine2010,11,1:1
15Treatments to control Phtrma and Alternaria infections of brassica seeds显示文摘Maude R B Humpherson-Jones F M Shuring C G 1984Plant Pathology1984,33,:1
16Smategies for control of seed-brne Alternaria dauci (leaf blight) of carrots in priming and process engineering systems 显示文摘Maude R B Drew R L K Gray D 1992Plant Pathology1992,41,2:1
17AB046.The Endocytic Adaptor Protein Numb Functions in Müller Glia to Maintain Retinal Polarity and Photoreceptor Survival through the Polarity Determinant Crumbs显示文摘Background:The loss of cell polarity plays a key part in retinal dystrophies such as retinitis pigmentosa(RP)and Leber congenital amaurosis(LCA),resulting in photoreceptor(PR)degeneration and vision loss.Despite not knowing the direct genotype-to-phenotype correlation,many disease-causing mutations in the polarity determinant Crumbs(Crb1),have been identified.Indeed,the loss of Crb1 in mice was shown to cause PR death,due to the loss of adhesions between PR and Müller cells at the apical surface of the retina.Unfortunately,although the role of Crb1 in neuron polarity and survival is well established,little is known about how its intracellular trafficking is regulated.With future treatments for retinal degenerative diseases in mind,the goal of this project is to understand the mechanism by which Crb1 is regulated and how it maintains retinal integrity.Previous work in our laboratory showed that Numb,an endocytic adaptor protein,is an important regulator of protein trafficking in retinal cells.We therefore hypothesized that Numb might function as regulator of Crb1 in Müller glia.Methods:To study Numb function in Müller cells,we generated a conditional knockout(cKO)mouse line to inactivate Numb specifically in Müller cells by crossing a Glast-CreERT2 mouse line with a Numb-floxed line.At 30 days,mice were administered tamoxifen to trigger inactivation of Numb and retinas were then collected at time points varying from 2 weeks to 17 months for analysis.Firstly,we studied the retinal morphology and outer limiting membrane integrity by histology and immunohistochemistry.Using electron microscopy(EM),adhesions between Müller glia and photoreceptors were analysed and retinal function was assayed in live mice by electroretinography(ERG).To detect protein expression levels,protein extracts were prepared from cKO and control retinas for immunoblotting.To test for the presence of a biochemical interaction,Hek-293 cells were transfected with Numb and Crb1 vectors,and protein extracts were processed for co-immunoprecipitation.Results:When Numb was deleted in Müller cells,we observed a similar retinal phenotype than what was reported in the Crb1 KO.In 3-month-old animals,we found a disruption of the outer limiting membrane and an ingression of photoreceptor cells in the inner layers of the retina.In older animals(17 months),we observed a clear thinning of the photoreceptor layer and reduced ERG responses.Immunoblotting of retinal lysates revealed that Numb cKO retinas had significantly lower expression of Crb1,suggesting that Numb function in Müller cells is critical to maintain Crb1 levels and thereby outer limiting membrane integrity.Interestingly,we found that Numb can interact with Crb1 both in vitro and in vivo,suggesting that Numb might function as an adaptor protein regulating Crb1 trafficking.Conclusions:Based on these results,we suggest that,in the absence of Numb,Crb1 cannot be trafficked to the apical membrane of Müller cells,and is instead degraded.This ruptures the adhesion between Müller and photoreceptor cells,leading to photoreceptor degeneration.We anticipate that understanding the mechanisms by which Crb1 maintains the structural integrity of the retina will lead to new possibilities for target-based therapies against retinal dystrophies.Maude Vinette Marie-Claude Bélanger Christine Jolicoeur Mina Gabraie Pierre Lachapelle Michel Cayouette 2019Annals of Eye Science2019,,1:0
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