排序方式: 共有29条查询结果,搜索用时 15 毫秒
1.
S. Shiozawa K. Shiozawa S. Shimizu Y. Tanaka I. Morimoto Y. Kuroki R. Yoshihara T. Fujita 《Cellular and molecular life sciences : CMLS》1989,45(8):764-765
Summary A sensitive radioimmunoassay showed that circulating -interferon in the plasma of healthy individuals was low in children and reached the highest level in the young adult, then declined gradually with age. Circulating -interferon was 0.201±0.059 ng/ml in males (n=19) and 0.184±0.076 ng/ml in females (n=14) at ages 30–39 years old. It was noted that circulating -interferon was maintained up to a certain level even in elderly individuals. 相似文献
2.
Wan J Yourshaw M Mamsa H Rudnik-Schöneborn S Menezes MP Hong JE Leong DW Senderek J Salman MS Chitayat D Seeman P von Moers A Graul-Neumann L Kornberg AJ Castro-Gago M Sobrido MJ Sanefuji M Shieh PB Salamon N Kim RC Vinters HV Chen Z Zerres K Ryan MM Nelson SF Jen JC 《Nature genetics》2012,44(6):704-708
RNA exosomes are multi-subunit complexes conserved throughout evolution and are emerging as the major cellular machinery for processing, surveillance and turnover of a diverse spectrum of coding and noncoding RNA substrates essential for viability. By exome sequencing, we discovered recessive mutations in EXOSC3 (encoding exosome component 3) in four siblings with infantile spinal motor neuron disease, cerebellar atrophy, progressive microcephaly and profound global developmental delay, consistent with pontocerebellar hypoplasia type 1 (PCH1; MIM 607596). We identified mutations in EXOSC3 in an additional 8 of 12 families with PCH1. Morpholino knockdown of exosc3 in zebrafish embryos caused embryonic maldevelopment, resulting in small brain size and poor motility, reminiscent of human clinical features, and these defects were largely rescued by co-injection with wild-type but not mutant exosc3 mRNA. These findings represent the first example of an RNA exosome core component gene that is responsible for a human disease and further implicate dysregulation of RNA processing in cerebellar and spinal motor neuron maldevelopment and degeneration. 相似文献
3.
4.
Nishimoto S Kawane K Watanabe-Fukunaga R Fukuyama H Ohsawa Y Uchiyama Y Hashida N Ohguro N Tano Y Morimoto T Fukuda Y Nagata S 《Nature》2003,424(6952):1071-1074
The eye lens is composed of fibre cells, which develop from the epithelial cells on the anterior surface of the lens. Differentiation into a lens fibre cell is accompanied by changes in cell shape, the expression of crystallins and the degradation of cellular organelles. The loss of organelles is believed to ensure the transparency of the lens, but the molecular mechanism behind this process is not known. Here we show that DLAD ('DNase II-like acid DNase', also called DNase IIbeta) is expressed in human and murine lens cells, and that mice deficient in the DLAD gene are incapable of degrading DNA during lens cell differentiation--the undigested DNA accumulates in the fibre cells. The DLAD-/- mice develop cataracts of the nucleus lentis, and their response to light on electroretinograms is severely reduced. These results indicate that DLAD is responsible for the degradation of nuclear DNA during lens cell differentiation, and that if DNA is left undigested in the lens, it causes cataracts of the nucleus lentis, blocking the light path. 相似文献
5.
6.
Location of functional regions of acetylcholine receptor alpha-subunit by site-directed mutagenesis 总被引:1,自引:0,他引:1
M Mishina T Tobimatsu K Imoto K Tanaka Y Fujita K Fukuda M Kurasaki H Takahashi Y Morimoto T Hirose 《Nature》1985,313(6001):364-369
The availability of cloned cDNAs encoding the four subunits of the Torpedo acetylcholine receptor, which can be expressed to make functional receptors in Xenopus oocytes, has made possible a detailed investigation of the functions of the different structural components of the receptor. The functional analysis of receptors with alpha-subunits altered at specific sites by site-directed mutagenesis of the cDNA has allowed the location of specific regions of the alpha-subunit molecule involved in acetylcholine binding and forming a transmembrane ionic channel. 相似文献
7.
用改良的Kepes磷酸饥饿法诱导大肠杆菌K—12AM1264同步化生长,细胞经8轮同步化步骤后可在磷酸不限制培养基中自由生长保持2~3次同步化细胞周期。K—12AM1264大肠杆菌的细胞增倍和分化周期分别为55和15min,同步化细胞周期可分达3个时相。细胞分裂期(P),细胞分裂和染色体复制起始间期(Q)以及染色体复制起始和细胞分裂间期(R)。R期又可分R1和R2两个亚期。在R1亚期胸腺呼啶掺入DNA的速度增加,在R2亚期掺入速度保持恒定。R1和R2期分别为15和10min。 相似文献
8.
9.
Cyclosporine induces cancer progression by a cell-autonomous mechanism 总被引:61,自引:0,他引:61
Hojo M Morimoto T Maluccio M Asano T Morimoto K Lagman M Shimbo T Suthanthiran M 《Nature》1999,397(6719):530-534
Malignancy is a common and dreaded complication following organ transplantation. The high incidence of neoplasm and its aggressive progression, which are associated with immunosuppressive therapy, are thought to be due to the resulting impairment of the organ recipient's immune-surveillance system. Here we report a mechanism for the heightened malignancy that is independent of host immunity. We show that cyclosporine (cyclosporin A), an immunosuppressant that has had a major impact on improving patient outcome following organ transplantation, induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Our studies show that cyclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruffling and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. These changes are prevented by treatment with monoclonal antibodies directed at transforming growth factor-beta (TGF-beta). In vivo, cyclosporine enhances tumour growth in immunodeficient SCID-beige mice; anti-TGF-beta monoclonal antibodies but not control antibodies prevent the cyclosporine-induced increase in the number of metastases. Our findings suggest that immunosuppressants like cyclosporine can promote cancer progression by a direct cellular effect that is independent of its effect on the host's immune cells, and that cyclosporine-induced TGF-beta production is involved in this. 相似文献