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Krishnan KJ Reeve AK Samuels DC Chinnery PF Blackwood JK Taylor RW Wanrooij S Spelbrink JN Lightowlers RN Turnbull DM 《Nature genetics》2008,40(3):275-279
Mitochondrial DNA (mtDNA) deletions are a primary cause of mitochondrial disease and are likely to have a central role in the aging of postmitotic tissues. Understanding the mechanism of the formation and subsequent clonal expansion of these mtDNA deletions is an essential first step in trying to prevent their occurrence. We review the previous literature and recent results from our own laboratories, and conclude that mtDNA deletions are most likely to occur during repair of damaged mtDNA rather than during replication. This conclusion has important implications for prevention of mtDNA disease and, potentially, for our understanding of the aging process. 相似文献
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Recent work suggests that an autosomal dominant gene for schizophrenia may be located on the 5q11-q13 region of chromosome 5 (refs 1 and 2): a report of schizophrenia associated with trisomy 5q11-q13 in two members of a family of Chinese origin prompted the discovery of linkage with markers p105-599Ha and p105-153Ra in five Icelandic and two English schizophrenic families. The strongest linkage was observed when the phenotype was broadly defined to include minor psychiatric diagnoses not traditionally considered part of the schizophrenia spectrum. By contrast, no evidence was found of linkage in a single multiplex Swedish schizophrenic pedigree. To determine whether these conflicting results arise from genetic and/or uncertainties in defining the schizophrenic phenotype, we examined fifteen Scottish schizophrenic families with restriction fragment length polymorphisms that span this region. We found no evidence for linkage, regardless of how broadly or narrowly the schizophrenic phenotype is defined, and conclude that a susceptibility locus, whose presence awaits confirmation, on the proximal portion of the long arm of chromosome 5 can be responsible for only a minority of cases of familial schizophrenia. 相似文献
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Myc and Max proteins possess distinct transcriptional activities. 总被引:68,自引:0,他引:68
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R. G. MacDonald R. H. McCusker D. J. Blackwood J. A. Vanderhoof J. H. Y. Park 《Cellular and molecular life sciences : CMLS》1998,54(2):158-166
To determine if intestinal stromal cells secrete diffusible factors such as insulin-like growth factors (IGFs) capable of
regulating epithelial cell growth in vitro, stromal cells were isolated by enzymatic digestion of rat intestine. Incorporation
of [3H]thymidine into DNA and [14C]leucine into protein of IEC-6 cells, a model intestinal epithelial cell line, was significantly increased (two- to threefold)
when the IEC-6 cells were co-cultured with stromal cells, relative to IEC-6 cells grown alone. Medium conditioned by stromal
cells stimulated DNA synthesis of IEC-6 cells in a dose-dependent manner. Analysis of the conditioned medium revealed that
intestinal stromal cells secreted IGF-I, but little IGF-II, in addition to an M
r 32,000 IGF-binding protein (IGFBP-2) and an IGFBP having M
r∼ 24,000. We conclude that rat intestinal stromal cells secrete one or more diffusible factors, which may include IGF-I and
IGFBPs, capable of stimulating proliferation of IEC-6 cells in vitro.
Received 25 August 1997; received after revision 7 November 1997; accepted 20 November 1997 相似文献
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R. A. Blackwood J. O. Cantor J. Moret I. Mandl 《Cellular and molecular life sciences : CMLS》1984,40(5):480-481
Summary Incorporation of [35]S-sulfate into hepatic glycosaminoglycans (GAGs) is affected by intravenous administration of endotoxin. There are significant increases in total labeled glycosaminoglycans and in the percentage of labeled dermatan sulfate 72 h post-endotoxin. 相似文献
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Assembly of microarrays for genome-wide measurement of DNA copy number. 总被引:20,自引:0,他引:20
A M Snijders N Nowak R Segraves S Blackwood N Brown J Conroy G Hamilton A K Hindle B Huey K Kimura S Law K Myambo J Palmer B Ylstra J P Yue J W Gray A N Jain D Pinkel D G Albertson 《Nature genetics》2001,29(3):263-264
We have assembled arrays of approximately 2,400 BAC clones for measurement of DNA copy number across the human genome. The arrays provide precise measurement (s.d. of log2 ratios=0.05-0.10) in cell lines and clinical material, so that we can reliably detect and quantify high-level amplifications and single-copy alterations in diploid, polyploid and heterogeneous backgrounds. 相似文献
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