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51.
One-stop shop for microarray data 总被引:8,自引:0,他引:8
52.
Canman JC Cameron LA Maddox PS Straight A Tirnauer JS Mitchison TJ Fang G Kapoor TM Salmon ED 《Nature》2003,424(6952):1074-1078
Proper positioning of the cell division plane during mitosis is essential for determining the size and position of the two daughter cells--a critical step during development and cell differentiation. A bipolar microtubule array has been proposed to be a minimum requirement for furrow positioning in mammalian cells, with furrows forming at the site of microtubule plus-end overlap between the spindle poles. Observations in other species have suggested, however, that this may not be true. Here we show, by inducing mammalian tissue cells with monopolar spindles to enter anaphase, that furrow formation in cultured mammalian cells does not require a bipolar spindle. Unexpectedly, cytokinesis occurs at high frequency in monopolar cells. Division always occurs at a cortical position distal to the chromosomes. Analysis of microtubules during cytokinesis in cells with monopolar and bipolar spindles shows that a subpopulation of stable microtubules extends past chromosomes and binds to the cell cortex at the site of furrow formation. Our data are consistent with a model in which chromosomes supply microtubules with factors that promote microtubule stability and furrowing. 相似文献
53.
Carpten JD Robbins CM Villablanca A Forsberg L Presciuttini S Bailey-Wilson J Simonds WF Gillanders EM Kennedy AM Chen JD Agarwal SK Sood R Jones MP Moses TY Haven C Petillo D Leotlela PD Harding B Cameron D Pannett AA Höög A Heath H James-Newton LA Robinson B Zarbo RJ Cavaco BM Wassif W Perrier ND Rosen IB Kristoffersson U Turnpenny PD Farnebo LO Besser GM Jackson CE Morreau H Trent JM Thakker RV Marx SJ Teh BT Larsson C Hobbs MR 《Nature genetics》2002,32(4):676-680
We report here the identification of a gene associated with the hyperparathyroidism-jaw tumor (HPT-JT) syndrome. A single locus associated with HPT-JT (HRPT2) was previously mapped to chromosomal region 1q25-q32. We refined this region to a critical interval of 12 cM by genotyping in 26 affected kindreds. Using a positional candidate approach, we identified thirteen different heterozygous, germline, inactivating mutations in a single gene in fourteen families with HPT-JT. The proposed role of HRPT2 as a tumor suppressor was supported by mutation screening in 48 parathyroid adenomas with cystic features, which identified three somatic inactivating mutations, all located in exon 1. None of these mutations were detected in normal controls, and all were predicted to cause deficient or impaired protein function. HRPT2 is a ubiquitously expressed, evolutionarily conserved gene encoding a predicted protein of 531 amino acids, for which we propose the name parafibromin. Our findings suggest that HRPT2 is a tumor-suppressor gene, the inactivation of which is directly involved in predisposition to HPT-JT and in development of some sporadic parathyroid tumors. 相似文献
54.
Effects of sympathetic stimulation on ventricular refractory periods in cats with acute coronary artery ligation 总被引:1,自引:0,他引:1
Ventricular refractory periods shorten in the ischemic area following acute coronary artery ligation. Subsequent bilateral sympathetic nerve stimulation reduces disparity in refractory periods across normal, border (peri-ischemic) and ischemic areas. 相似文献
55.
Many invertebrates and vertebrates are sensitive to the polarization of light. The biophysical basis of invertebrate polarization sensitivity is an intrinsic dichroism, the alignment of chromophores along the photoreceptor microvilli. But such dichroism to axially propagating light is not present in vertebrate photoreceptors, whose chromophores are free to rotate in the plane of the outer-segment disc membranes, and a biophysical mechanism responsible for vertebrate polarization sensitivity has not been established. We hypothesize that the roughly elliptical cross-sectioned double-cone inner segment acts as a birefringent, polarization-sensitive dielectric waveguide, and that the double cone mosaic generates a 'polarization contrast' neural image. Here we confirm three predictions derived from these hypotheses: (1) 90 degrees periodicity for polarization sensitivity; (2) polarization sensitivity maxima corresponding to the absolute orientation of the axes of the double-cone inner-segment cross-sections; and (3) action spectrum for polarization sensitivity corresponding to the absorption spectrum of the double cones. We also present evidence for a polarization-opponent neural encoding in vertebrates. 相似文献
56.
p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation 总被引:1,自引:0,他引:1
57.
Nuclear variation between diploid angiosperms 总被引:6,自引:0,他引:6
58.
59.
Glioblastoma stem-like cells give rise to tumour endothelium 总被引:2,自引:0,他引:2
Wang R Chadalavada K Wilshire J Kowalik U Hovinga KE Geber A Fligelman B Leversha M Brennan C Tabar V 《Nature》2010,468(7325):829-833
Glioblastoma (GBM) is among the most aggressive of human cancers. A key feature of GBMs is the extensive network of abnormal vasculature characterized by glomeruloid structures and endothelial hyperplasia. Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined. Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7. We additionally demonstrate that the stem-cell-like CD133(+) fraction includes a subset of vascular endothelial-cadherin (CD144)-expressing cells that show characteristics of endothelial progenitors capable of maturation into endothelial cells. Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell. The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium. Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors. These data may provide new perspectives on the mechanisms of failure of anti-angiogenesis inhibitors currently in use. The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis. 相似文献
60.
Phagocytosis promotes programmed cell death in C. elegans. 总被引:14,自引:0,他引:14
In the nematode Caenorhabditis elegans programmed cell death requires the killer genes egl-1, ced-4 and ced-3 (refs 1 and 2), and the engulfment of dying cells requires the genes ced-1, ced-2, ced-5, ced-6, ced-7, ced-10 and ced-12 (refs 3,4,5). Here we show that engulfment promotes programmed cell death. Mutations that cause partial loss of function of killer genes allow the survival of some cells that are programmed to die, and mutations in engulfment genes enhance the frequency of this cell survival. Furthermore, mutations in engulfment genes alone allow the survival and differentiation of some cells that would normally die. Engulfment genes probably act in engulfing cells to promote death, as the expression in engulfing cells of ced-1, which encodes a receptor that recognizes cell corpses, rescues the cell-killing defects of ced-1 mutants. We propose that engulfing cells act to ensure that cells triggered to undergo programmed cell death by the CED-3 caspase die rather than recover after the initial stages of death. 相似文献