全文获取类型
收费全文 | 115篇 |
免费 | 9篇 |
出版年
2021年 | 3篇 |
2020年 | 1篇 |
2018年 | 2篇 |
2017年 | 1篇 |
2015年 | 4篇 |
2014年 | 3篇 |
2013年 | 5篇 |
2012年 | 6篇 |
2011年 | 5篇 |
2010年 | 4篇 |
2009年 | 3篇 |
2008年 | 1篇 |
2007年 | 7篇 |
2006年 | 5篇 |
2005年 | 4篇 |
2004年 | 7篇 |
2003年 | 3篇 |
2002年 | 3篇 |
2001年 | 5篇 |
2000年 | 5篇 |
1999年 | 6篇 |
1998年 | 10篇 |
1997年 | 3篇 |
1996年 | 2篇 |
1995年 | 2篇 |
1994年 | 4篇 |
1993年 | 4篇 |
1991年 | 1篇 |
1990年 | 1篇 |
1989年 | 2篇 |
1988年 | 1篇 |
1986年 | 1篇 |
1985年 | 1篇 |
1984年 | 4篇 |
1983年 | 2篇 |
1977年 | 1篇 |
1974年 | 1篇 |
1972年 | 1篇 |
排序方式: 共有124条查询结果,搜索用时 46 毫秒
81.
82.
Previously it has been shown that insulin-mediated tyrosine phosphorylation of myosin heavy chain is concomitant with enhanced association of C-terminal SRC kinase during skeletal muscle differentiation. We sought to identify putative site(s) for this phosphorylation event. A combined bioinformatics approach of motif prediction and evolutionary and structural analyses identified tyrosines163 and 1856 of the skeletal muscle heavy chain as the leading candidate for the sites of insulin-mediated tyrosine phosphorylation. Our work is suggestive that tyrosine phosphorylation of myosin heavy chain, whether in skeletal muscle or in platelets, is a significant event that may initiate cytoskeletal reorganization of muscle cells and platelets. Our studies provide a good starting point for further functional analysis of MHC phosphor-signalling events within different cells. 相似文献
83.
High frequency hearing loss correlated with mutations in the GJB2 gene 总被引:18,自引:0,他引:18
Wilcox SA Saunders K Osborn AH Arnold A Wunderlich J Kelly T Collins V Wilcox LJ McKinlay Gardner RJ Kamarinos M Cone-Wesson B Williamson R Dahl HH 《Human genetics》2000,106(4):399-405
Genetic hearing impairment affects approximately 1/2000 live births. Mutations in one gene, GJB2, coding for connexin 26 cause 10%-20% of all genetic sensorineural hearing loss. Mutation analysis in the GJB2 gene and audiology were performed on 106 families presenting with at least one child with congenital hearing loss. The families were recruited from a hospital-based multidisciplinary clinic, which functions to investigate the aetiology of sensorineural hearing loss in children and which serves an ethnically diverse population. In 74 families (80 children), the aetiology was consistent with non-syndromic recessive hearing loss. Six different connexin 26 mutations, including one novel mutation, were identified. We show that GJB2 mutations cause a range of phenotypes from mild to profound hearing impairment and that loss of hearing in the high frequency range (4000-8000 Hz) is a characteristic feature in children with molecularly diagnosed connexin 26 hearing impairment. We also demonstrate that this type of audiology and high frequency hearing loss is found in a similar-sized group of deaf children in whom a mutation could only be found in one of the connexin 26 alleles, suggesting connexin 26 involvement in the aetiology of hearing loss in these cases. In our study of the M34T mutation, only compound heterozygotes exhibited hearing loss, suggesting autosomal recessive inheritance. 相似文献
84.
Defective neurogenesis in citron kinase knockout mice by altered cytokinesis and massive apoptosis 总被引:12,自引:0,他引:12
Di Cunto F Imarisio S Hirsch E Broccoli V Bulfone A Migheli A Atzori C Turco E Triolo R Dotto GP Silengo L Altruda F 《Neuron》2000,28(1):115-127
Citron-kinase (Citron-K) has been proposed by in vitro studies as a crucial effector of Rho in regulation of cytokinesis. To further investigate in vivo its biologic functions, we have inactivated Citron-K gene in mice by homologous recombination. Citron-K-/- mice grow at slower rates, are severely ataxic, and die before adulthood as a consequence of fatal seizures. Their brains display defective neurogenesis, with depletion of specific neuronal populations. These abnormalities arise during development of the central nervous system due to altered cytokinesis and massive apoptosis. Our results indicate that Citron-K is essential for cytokinesis in vivo but only in specific neuronal precursors. Moreover, they suggest a novel molecular mechanism for a subset of human malformative syndromes of the CNS. 相似文献
85.
86.
87.
88.
Molecular phylogenetics of Stenodermatini bat genera: congruence of data from nuclear and mitochondrial DNA 总被引:2,自引:1,他引:1
Van den Bussche RA; Baker RJ; Wichman HA; Hamilton MJ 《Molecular biology and evolution》1993,10(5):944-959
Within the tribe Stenodermatini the systematics of the complex of species
allied with the genus Artibeus has generated several alternative
phylogenetic hypotheses. The most recent treatment recognized four genera
(Artibeus, Dermanura, Enchisthenes, and Koopmania) and suggested that the
most recent common ancestor of these four genera would include the common
ancestor of all other currently recognized Stenodermatini genera except
Sturnira. To test this hypothesis, we examined an EcoRI-defined nuclear
satellite DNA repeat and 402 bp of DNA sequence variation from the
mitochondrial cytochrome b gene. Phylogenetic conclusions based on Southern
blot analyses, in situ hybridization, and mitochondrial DNA sequence data
indicate that Enchisthenes is not closely related to Dermanura, Artibeus,
or Koopmania and that Dermanura, Artibeus, and Koopmania shared a common
ancestor after diverging from the remainder of the Stenodermatini. If our
conclusions are correct, then justification for recognizing Dermanura and
Koopmania as generically distinct from Artibeus must be based on the
magnitude of difference that distinguishes each rather than on the
conclusion that to place them as congeneric with Artibeus creates a
paraphyletic taxon.
相似文献
89.
90.