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Autophagy is a cellular process in degradation of long-lived proteins and organelles in the cytosol for maintaining cellular
homeostasis, which has been linked to a wide range of human health and disease states, including viral infection. The viral
infected cells exhibit a complicated cross-talking between autophagy and virus. It has been shown that autophagy interacts
with both adaptive and innate immunity. For adaptive immunity, viral antigens can be processed in autophagosomes by acidic
proteases before major histocompatibility complex (MHC) class II presentation. For innate immunity, autophagy may assist in
the delivery of viral nucleic acids to endosomal TLRs and also functions as a part of the TLR-or-PKR-downstream responses.
Autophagy was also reported to suppress the magnitude of host innate antiviral immunity in certain cases. On the other hand,
viruses has evolved many strategies to combat or utilize the host autophagy for their own benefit. In this review we discussed
recent advances toward clarifying the cross-talking between autophagy and viral infection in mammalian cells. 相似文献
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Xinxian Qiao Liyong Zhang Armin M Gamper Takeo Fujita Yong Wan 《Cell cycle (Georgetown, Tex.)》2010,9(19):3904-3912
Anaphase-promoting complex/cyclosome (APC/C) is a multifunctional ubiquitin-protein ligase that targets various substrates for proteolysis inside and outside of the cell cycle. The activation of APC/C is dependent on two WD-40 domain proteins, Cdc20 and Cdh1. While APC/Cdc20 principally regulates mitotic progression, APC/Cdh1 shows a broad spectrum of substrates in and beyond cell cycle. In the past several years, numerous biochemical and mouse genetic studies have greatly attracted our attention to the emerging role of APC/Cdh1 in genomic integrity, cellular differentiation and human diseases. This review will aim to summarize the recently expanded understanding of APC/Cdh1 in regulating biological function and how its dysfunction may lead to diseases.Key words: APC/C, Cdh1, proteolysis, genomic integrity, signal transduction, differentiation, tumorigenesis 相似文献
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How the mechanisms of dosage compensation distinguish the sex chromosomes from the autosomes has been something of a mystery. A recent study in Caenorhabditis elegans has identified clusters of two common DNA motifs as a cis-acting code for the recruitment of the DCC, the protein complex that mediates dosage compensation. 相似文献
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抗风湿新药白芍总甙的工艺研究 总被引:3,自引:0,他引:3
从白芍中提得的抗风湿性活性组分——白芍总甙(TGP)为新的临床推广用药,本文对其生产工艺进行了改进,简述了采用的新的方法和程序,使TGP得率由原有的3%提高到大于5%,成本大大降低,有利于该产品的大量生产及其广泛使用。 相似文献
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Xinxian Deng Di Kim Nguyen R. Scott Hansen Daniel L. Van Dyke Stanley M. Gartler Christine M. Disteche 《PLoS genetics》2009,5(12)
In mammals, dosage compensation is achieved by doubling expression of X-linked genes in both sexes, together with X inactivation in females. Up-regulation of the active X chromosome may be controlled by DNA sequence–based and/or epigenetic mechanisms that double the X output potentially in response to autosomal factor(s). To determine whether X expression is adjusted depending on ploidy, we used expression arrays to compare X-linked and autosomal gene expression in human triploid cells. While the average X:autosome expression ratio was about 1 in normal diploid cells, this ratio was lower (0.81–0.84) in triploid cells with one active X and higher (1.32–1.4) in triploid cells with two active X''s. Thus, overall X-linked gene expression in triploid cells does not strictly respond to an autosomal factor, nor is it adjusted to achieve a perfect balance. The unbalanced X:autosome expression ratios that we observed could contribute to the abnormal phenotypes associated with triploidy. Absolute autosomal expression levels per gene copy were similar in triploid versus diploid cells, indicating no apparent global effect on autosomal expression. In triploid cells with two active X''s our data support a basic doubling of X-linked gene expression. However, in triploid cells with a single active X, X-linked gene expression is adjusted upward presumably by an epigenetic mechanism that senses the ratio between the number of active X chromosomes and autosomal sets. Such a mechanism may act on a subset of genes whose expression dosage in relation to autosomal expression may be critical. Indeed, we found that there was a range of individual X-linked gene expression in relation to ploidy and that a small subset (∼7%) of genes had expression levels apparently proportional to the number of autosomal sets. 相似文献
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Dosage compensation modulates global expression of an X chromosome and is necessary to restore the balance between X-chromosome and autosome expression in both sexes. A central question in the field is how this regulation is directed. Large non-coding RNAs, such as Xist in mammals and roX in flies, have pivotal roles in targeting chromosome-wide modification for dosage compensation. Several recent studies in Drosophila provide new insight into the principles of X-chromosome recognition and the function of non-coding RNA in this process. 相似文献