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排序方式: 共有4257条查询结果,搜索用时 15 毫秒
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Jorge E Osorio Ivan D Velez Cynthia Thomson Liliana Lopez Alejandra Jimenez Aurelia A Haller Shawn Silengo Jaclyn Scott Karen L Boroughs Janae L Stovall Betty E Luy John Arguello Mark E Beatty Joseph Santangelo Gilad S Gordon Claire Y-H Huang Dan T Stinchcomb 《The Lancet infectious diseases》2014,14(9):830-838
74.
Emily M. Darrow Andrew P. Seberg Sunny Das Debbie M. Figueroa Zhuo Sun Shawn C. Moseley Brian P. Chadwick 《Chromosome research》2014,22(3):335-350
Euchromatic features are largely absent from the human inactive X chromosome (Xi), with the exception of several large tandem repeats that can be detected as euchromatin bands at metaphase. Despite residing megabases apart, these tandem repeats make frequent inactive X-specific interactions. The mouse homologue has been reported for at least one of the tandem repeats, but whether the mouse Xi is also characterized by distinct bands of euchromatin remains unknown. We examined the mouse Xi for the presence of euchromatin bands by examining the pattern of histone H3 dimethylated at lysine 4 and detected two major signals. The first band resides in the subtelomeric region of band XF5 and may correspond to the pseudoautosomal region. The second band localizes to XE3 and coincides with an extensive complex repeat composed of a large tandem and inverted repeat segment as well as several large short interspersed nuclear element (SINE)-rich tandem repeats. Fluorescence in situ hybridization reveals that sequences with homology to the repeat region are scattered along the length of the Y chromosome. Immunofluorescence analysis of histone H3 trimethylated at lysine 9 on metaphase chromosomes indicates that the repeat region corresponds to a band of constitutive heterochromatin on the male X and female active X chromosomes, whereas the euchromatin signal appears to be female specific. These data suggest that the band of euchromatin observed at XE3 is unique to the mouse Xi, comparable to the chromatin arrangement of several large tandem repeats located on the human X chromosome. 相似文献
75.
Martin Picard Jiangwen Zhang Saege Hancock Olga Derbeneva Ryan Golhar Pawel Golik Sean O’Hearn Shawn Levy Prasanth Potluri Maria Lvova Antonio Davila Chun Shi Lin Juan Carlos Perin Eric F. Rappaport Hakon Hakonarson Ian A. Trounce Vincent Procaccio Douglas C. Wallace 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(38):E4033-E4042
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Jerry H. Gurwitz MD Terry S. Field DSc Jessica Ogarek MS Jennifer Tjia MD MSCE Sarah L. Cutrona MD MPH Leslie R. Harrold MD MPH Shawn J. Gagne BA Peggy Preusse RN Jennifer L. Donovan PharmD Abir O. Kanaan PharmD George Reed PhD Lawrence Garber MD 《Journal of the American Geriatrics Society》2014,62(5):865-871
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Lou X Fan F Messa M Raimondi A Wu Y Looger LL Ferguson SM De Camilli P 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(8):E515-E523
Endocytic recycling of synaptic vesicles after exocytosis is critical for nervous system function. At synapses of cultured neurons that lack the two "neuronal" dynamins, dynamin 1 and 3, smaller excitatory postsynaptic currents are observed due to an impairment of the fission reaction of endocytosis that results in an accumulation of arrested clathrin-coated pits and a greatly reduced synaptic vesicle number. Surprisingly, despite a smaller readily releasable vesicle pool and fewer docked vesicles, a strong facilitation, which correlated with lower vesicle release probability, was observed upon action potential stimulation at such synapses. Furthermore, although network activity in mutant cultures was lower, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity was unexpectedly increased, consistent with the previous report of an enhanced state of synapsin 1 phosphorylation at CaMKII-dependent sites in such neurons. These changes were partially reversed by overnight silencing of synaptic activity with tetrodotoxin, a treatment that allows progression of arrested endocytic pits to synaptic vesicles. Facilitation was also counteracted by CaMKII inhibition. These findings reveal a mechanism aimed at preventing synaptic transmission failure due to vesicle depletion when recycling vesicle traffic is backed up by a defect in dynamin-dependent endocytosis and provide new insight into the coupling between endocytosis and exocytosis. 相似文献
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Christ SE Moffitt AJ Peck D White DA Hilgard J 《Journal of inherited metabolic disease》2012,35(5):807-816
Previous histological and neuroimaging studies have documented structural abnormalities in the white matter of the brain in individuals with early-treated phenylketonuria (ETPKU). It remains unclear, however, the extent to which the function of the brain's interconnections are impacted by this condition. Presently, we utilized functional magnetic resonance imaging (fMRI) to evaluate the synchronization of neural signals (i.e., functional connectivity) among brain regions comprising the default mode network (DMN) in a sample of 11 individuals with ETPKU and 11 age- and gender-matched neurologically intact controls. The DMN is a group of interconnected brain regions that are known to be generally more active during rest than during task performance. Data analysis revealed decreased functional connectivity among DMN regions for the ETPKU group compared with the control group. Within the PKU group, we also found a significant relationship between blood phenylalanine (phe) levels and the functional connectivity between select regions of the DMN. In conjunction with findings from another recent fMRI study (Christ, Moffitt et al. 2010), the present results suggest that ETPKU-related deficiencies in functional connectivity are pervasive. The current findings also provide initial evidence that the extent of such impairment may be moderated in part by blood phe levels. 相似文献