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Huntington’s disease (HD) is a devastating dominantly inherited neurodegenerative disorder caused by an abnormal polyglutamine expansion in the N-terminal part of the huntingtin (HTT) protein. HTT is a large scaffold protein that interacts with more than a hundred proteins and is probably involved in several cellular functions. The mutation is dominant, and is thought to confer new and toxic functions to the protein. However, there is emerging evidence that the mutation also alters HTT’s normal functions. Therefore, HD models need to recapitulate this duality if they are to be relevant. Drosophila melanogaster is a useful in vivo model, widely used to study HD through the overexpression of full-length or N-terminal fragments of mutant human HTT. However, it is unclear whether Drosophila huntingtin (DmHTT) shares functions similar to the mammalian HTT. Here, we used various complementary approaches to analyze the function of DmHTT in fast axonal transport. We show that DmHTT interacts with the molecular motor dynein, associates with vesicles and co-sediments with microtubules. DmHTT co-localizes with Brain-derived neurotrophic factor (BDNF)-containing vesicles in rat cortical neurons and partially replaces mammalian HTT in a fast axonal transport assay. DmHTT-KO flies show a reduced fast axonal transport of synaptotagmin vesicles in motoneurons in vivo. These results suggest that the function of HTT in axonal transport is conserved between flies and mammals. Our study therefore validates Drosophila melanogaster as a model to study HTT function, and its dysfunction associated with HD. 相似文献
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Fermin M. Sanchez-Guijo Juan F. Blanco Graciela Cruz Sandra Muntion Maria Gomez Soraya Carrancio Olga Lopez-Villar Maria-Victoria Barbado Luis-Ignacio Sanchez-Abarca Belén Blanco Jesus G. Briñon Maria-Consuelo del Cañizo 《Cell and tissue research》2009,336(3):501-507
Trabecular bone fragments from femoral heads are sometimes used as bone grafts and have been described as a source of mesenchymal
progenitor cells. Nevertheless, mesenchymal stromal cells (MSC) from trabecular bone have not been directly compared with
MSC obtained under standard conditions from iliac crest aspiration of the same patients. This is the ideal control to avoid
inter-individual variation. We have obtained MSC by a novel method (grinding bone fragments with a bone mill without enzymatic
digestion) from the femoral heads of 11 patients undergoing hip replacement surgery and compared them with MSC obtained by
standard iliac crest aspiration of bone marrow from the same patients. We have shown that trabecular bone MSC obtained by
mechanically fragmented femoral heads fulfil the immunophenotypic and multilineage (adipogenic, osteogenic and chondrogenic)
differentiation criteria used to define MSC. We have also differentially compared cellular yields, growth kinetics, cell cycle
assessment, and colony-forming unit-fibroblast content of MSC from both sources and conclude that these parameters do not
significantly differ. Nevertheless, the finding of slight differences, such as a higher expression of the immature marker
CD90, a lower expansion time through the different passages, and a higher percentage of cycling cells in the trabecular bone
MSC, warrants further studies with the isolation method proposed here in order to gain further knowledge of the status of
MSC in this setting.
The present study was partially supported by grant HUS01B07 from the Consejería de Educación and by grant SAN196/SA13/07 from
the Consejería de Sanidad, Junta de Castilla y León, Spain. 相似文献
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Guillermo Ruiz-Irastorza Nerea Olivares Ioana Ruiz-Arruza Agustin Martinez-Berriotxoa Maria-Victoria Egurbide Ciriaco Aguirre 《Arthritis research & therapy》2009,11(4):R109-8
Introduction
Infections commonly complicate the course of systemic lupus erythematosus (SLE). Our aim is to investigate the clinical predictors of major infections in patients with SLE. 相似文献6.
Ana Carolina Patrício de Albuquerque Sousa Ricardo Oliveira Guerra Mai Thanh Tu Susan P. Phillips Jack M. Guralnik Maria-Victoria Zunzunegui 《PloS one》2014,9(8)
Background
This study examines the associations between lifecourse adversity and physical performance in old age in different societies of North and South America and Europe.Methods
We used data from the baseline survey of the International Study of Mobility in Aging, conducted in: Kingston (Canada), Saint-Hyacinthe (Canada), Natal (Brazil), Manizales (Colombia) and Tirana (Albania). The study population was composed of community dwelling people between 65 and 74 years of age, recruiting 200 men and 200 women at each site. Physical Performance was assessed with the Short Physical Performance Battery (SPPB). Economic and social adversity was estimated from childhood adverse events, low education, semi-skilled occupations during adulthood and living alone and insufficient income in old age.Results
A total of 1995 people were assessed. Low physical performance was associated with childhood social and economic adversity, semi-skilled occupations, living alone and insufficient income. Physical performance was lower in participants living in Colombia, Brazil and Albania than in Canada counterparts, despite adjustment for lifecourse adversity, age and sex.Conclusions
We show evidence of the early origins of social and economic inequalities in physical performance during old age in distinct populations and for the independent and cumulative disadvantage of low socioeconomic status during adulthood and poverty and living alone in later life. 相似文献7.
Casimiro Barbado Manuel Ramírez M. Angel Blanco J. López-Barea Carmen Pueyo 《Current microbiology》1983,8(5):251-253
Mutants sensitive to moderate H2O2 concentrations were selected in a HfrphoA (S33)Escherichia coli strain after mutagenesis withN-methyl,N-nitro,N-nitrosoguanidine (NG). Of the sensitive strains, 31% were catalase-deficient and retained glutathione reductase levels similar to those of the parental strain, whereas 69% still had normal catalase and glutathione reductase activities. Mutants supersensitive to low H2O2 concentrations were selected in a catalase-deficient strain (CGR201) after mutagenesis with NG. Of these, 20% were glutathione reductase-deficient, and the remaining 80% were unaffected in this enzymatic activity. Compared with the parental strain S33, H2O2 was 5 to 12 times more toxic for the sensitive mutants, and 19 to 21 times for the supersensitive ones. 相似文献
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Ancellin N Preisser L Le Maout S Barbado M Créminon C Corman B Morel A 《Cellular signalling》1999,11(10):743-751
The vasopressin V1a receptor undergoes homologous and heterologous desensitizations which can be mimicked by activation of protein kinase C. This suggests that phosphorylation of the V1a receptor may be involved in the desensitization mechanisms. Such a phosphorylation was presently investigated in HEK 293 cells stably transfected with rat vasopressin V1a receptor. Metabolic labelling and immunoprecipitation of epitope-tagged V1a receptor evidenced a 52-kDa band and a 92-kDa band. Glycosidase treatments and immunoblotting experiments suggest that the 52-kDa band corresponds to an immature unprocessed receptor protein, whereas the 92-kDa band would correspond to a highly glycosylated form of the mature V1a receptor. Exposure of the cells to vasopressin induced a selective 32P phosphate incorporation in the 92-kDa form of the receptor. This homologous ligand-induced phosphorylation was dose dependent with maximal phosphate incorporation corresponding to four times the basal level. Stimulation of the endogenous phospholipase C-coupled m3 muscarinic receptor by carbachol-induced heterologous phosphorylation of the V1a receptor whose amplitude was half that of the homologous phosphorylation. This heterologous phosphorylation was associated with a reduced vasopressin-dependent increase in intracellular calcium. 相似文献
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