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排序方式: 共有138条查询结果,搜索用时 15 毫秒
1.
We tested the hypothesis that amyloid precursor protein (APP) and its relatives function as vesicular receptor proteins for kinesin-I. Deletion of the Drosophila APP-like gene (Appl) or overexpression of human APP695 or APPL constructs caused axonal transport phenotypes similar to kinesin and dynein mutants. Genetic reduction of kinesin-I expression enhanced while genetic reduction of dynein expression suppressed these phenotypes. Deletion of the C terminus of APP695 or APPL, including the kinesin binding region, disrupted axonal transport of APP695 and APPL and abolished the organelle accumulation phenotype. Neuronal apoptosis was induced only by overexpression of constructs containing both the C-terminal and Abeta regions of APP695. We discuss the possibility that axonal transport disruption may play a role in the neurodegenerative pathology of Alzheimer's disease. 相似文献
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3.
A highly conserved nuclear gene for low-level phylogenetics: elongation factor-1 alpha recovers morphology-based tree for heliothine moths 总被引:8,自引:2,他引:6
Cho S; Mitchell A; Regier JC; Mitter C; Poole RW; Friedlander TP; Zhao S 《Molecular biology and evolution》1995,12(4):650-656
Molecular systematists need increased access to nuclear genes. Highly
conserved, low copy number protein-encoding nuclear genes have attractive
features for phylogenetic inference but have heretofore been applied mostly
to very ancient divergences. By virtue of their synonymous substitutions,
such genes should contain a wealth of information about lower-level
taxonomic relationships as well, with the advantage that amino acid
conservatism makes both alignment and primer definition straightforward. We
tested this postulate for the elongation factor-1 alpha (EF-1 alpha) gene
in the noctuid moth subfamily Heliothinae, which has probably diversified
since the middle Tertiary. We sequenced 1,240 bp in 18 taxa representing
heliothine groupings strongly supported by previous morphological and
allozyme studies. The single most parsimonious gene tree and the
neighbor-joining tree for all nucleotides show almost complete concordance
with the morphological tree. Homoplasy and pairwise divergence levels are
low, transition/transversion ratios are high, and phylogenetic information
is spread evenly across gene regions. The EF-1 alpha gene and presumably
other highly conserved genes hold much promise for phylogenetics of
Tertiary age eukaryote groups.
相似文献
4.
Cultured chick embryo fibroblasts derived from skin and skeletal muscle exhibit hyaluronidase activity both associated with the cell layer and secreted into the medium. Although both forms of the enzyme have a number of similar characteristics (R.W. Orkin and B.P. Toole, 1980, J. Biol. CHem. 255), they differ in thermal stability at neutral pH and in behavior on ion-exchange chromatography. Both forms of the enzyme are equally stable at acidic pH for long intervals, but the cell-associated hyaluronidase is significantly less stable than the secreted froms at neutral pH and at temperatures more than or equal to 30 degrees C. Neither the presence of proteases nor inhibitors of hyaluronidase appear to be involved in the cell-asspcoated enzyme. Chromatography of the two forms of hyaluronidase on carboxymethyl cellulose reveals that most (60-90 percent) of the secreted form of the enzyme elutes at a lower ionic strength than the cell- associated enzyme. Treatment of the secreted form of hyaluronidase with neuraminidase shifts its elution profile on carboxymethyl cellulose toward that of the cell-associated form, and also decreases its thermal stability at neutral pH. In contrast, treatment of the secreted form of hyaluronidase with alkaline phosphatase has no detectable effect. These data suggest that the secreted hyaluronidase differs from the cellular form in possessing additional sialic acid residues which endow the former with increased stability in the extracellular milieu. 相似文献
5.
V R Edgerton G W Gardner Y Ohira K A Gunawardena B Senewiratne 《BMJ (Clinical research ed.)》1979,2(6204):1546-1549
The effects of iron-deficiency anaemia on workers productivity were studied in a tea plantation in Sri Lanka. The quantity of tea picked per day was studied before and after iron supplementation or placebo treatment. After one month''s treatment significantly more tea was picked when the haemoglobin (Hb) concentration was increased by iron supplementation than when it was not. The degree of improvement was greater in more-anaemic subjects (those with concentrations of 6.0-9.0 g Hb/dl). The level of physical activity of anaemic subjects in their everyday environment was also recorded for four or 24 hours continuously both before and after treatment. After three weeks these levels was significantly greater in the iron-treated than matched placebo-treated subjects. The economic implications of increased work productively with iron treatment are evident, particularly in developing countries. These results also provide strong evidence for the clinical impression that people with iron-deficiency anaemia suffer from tiredness and weakness. 相似文献
6.
Ling Xie Cui Liu Li Wang Harsha P. Gunawardena Yanbao Yu Ruyun Du Debra J. Taxman Penggao Dai Zhen Yan Jing Yu Stephen P. Holly Leslie V. Parise Yisong Y. Wan Jenny P. Ting Xian Chen 《Cell reports》2013,3(3):678-688
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7.
A PBX1 transcriptional network controls dopaminergic neuron development and is impaired in Parkinson's disease
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J Carlos Villaescusa Bingsi Li Enrique M Toledo Pia Rivetti di Val Cervo Shanzheng Yang Simon RW Stott Karol Kaiser Saiful Islam Daniel Gyllborg Rocio Laguna‐Goya Michael Landreh Peter Lönnerberg Anna Falk Tomas Bergman Roger A Barker Sten Linnarsson Licia Selleri Ernest Arenas 《The EMBO journal》2016,35(18):1963-1978
8.
Programmed cell death (PCD) functions in the developmental remodeling of leaf shape in higher plants, a process analogous to digit formation in the vertebrate limb. In this study, we provide a cytological characterization of the time course of events as PCD remodels young expanding leaves of the lace plant. Tonoplast rupture is the first PCD event in this system, indicated by alterations in cytoplasmic streaming, loss of anthocyanin color, and ultrastructural appearance. Nuclei become terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling positive soon afterward but do not become morphologically altered until late stages of PCD. Genomic DNA is fragmented, but not into internucleosomal units. Other cytoplasmic changes, such as shrinkage and degradation of organelles, occur later. This form of PCD resembles tracheary element differentiation in cytological execution but requires unique developmental regulation so that discrete panels of tissue located equidistantly between veins undergo PCD while surrounding cells do not. 相似文献
9.
Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila 总被引:6,自引:0,他引:6
Gunawardena S Her LS Brusch RG Laymon RA Niesman IR Gordesky-Gold B Sintasath L Bonini NM Goldstein LS 《Neuron》2003,40(1):25-40
We tested whether proteins implicated in Huntington's and other polyglutamine (polyQ) expansion diseases can cause axonal transport defects. Reduction of Drosophila huntingtin and expression of proteins containing pathogenic polyQ repeats disrupt axonal transport. Pathogenic polyQ proteins accumulate in axonal and nuclear inclusions, titrate soluble motor proteins, and cause neuronal apoptosis and organismal death. Expression of a cytoplasmic polyQ repeat protein causes adult retinal degeneration, axonal blockages in larval neurons, and larval lethality, but not neuronal apoptosis or nuclear inclusions. A nuclear polyQ repeat protein induces neuronal apoptosis and larval lethality but no axonal blockages. We suggest that pathogenic polyQ proteins cause neuronal dysfunction and organismal death by two non-mutually exclusive mechanisms. One mechanism requires nuclear accumulation and induces apoptosis; the other interferes with axonal transport. Thus, disruption of axonal transport by pathogenic polyQ proteins could contribute to early neuropathology in Huntington's and other polyQ expansion diseases. 相似文献
10.
Mathematical models are extensively employed to understand physicochemical processes in biological systems. In the absence of detailed mechanistic knowledge, models are often based on network inference methods, which in turn rely upon perturbations to nodes by biochemical means. We have discovered a potential pitfall of the approach underpinning such methods when applied to signaling networks. We first show experimentally, and then explain mathematically, how even in the simplest signaling systems, perturbation methods may lead to paradoxical conclusions: for any given pair of two components X and Y, and depending upon the specific intervention on Y, either an activation or a repression of X could be inferred. This effect is of a different nature from incomplete network identification due to underdetermined data and is a phenomenon intrinsic to perturbations. Our experiments are performed in an in vitro minimal system, thus isolating the effect and showing that it cannot be explained by feedbacks due to unknown intermediates. Moreover, our in vitro system utilizes proteins from a pathway in mammalian (and other eukaryotic) cells that play a central role in proliferation, gene expression, differentiation, mitosis, cell survival, and apoptosis. This pathway is the perturbation target of contemporary therapies for various types of cancers. The results presented here show that the simplistic view of intracellular signaling networks being made up of activation and repression links is seriously misleading, and call for a fundamental rethinking of signaling network analysis and inference methods. 相似文献