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Li G Alt FW Cheng HL Brush JW Goff PH Murphy MM Franco S Zhang Y Zha S 《Molecular cell》2008,31(5):631-640
Mutations in XLF/Cernunnos (XLF) cause lymphocytopenia in humans, and various studies suggest an XLF role in classical nonhomologous end joining (C-NHEJ). We now find that XLF-deficient mouse embryonic fibroblasts are ionizing radiation (IR) sensitive and severely impaired for ability to support V(D)J recombination. Yet mature lymphocyte numbers in XLF-deficient mice are only modestly decreased. Moreover, XLF-deficient pro-B lines, while IR-sensitive, perform V(D)J recombination at nearly wild-type levels. Correspondingly, XLF/p53-double-deficient mice are not markedly prone to the pro-B lymphomas that occur in previously characterized C-NHEJ/p53-deficient mice; however, like other C-NHEJ/p53-deficient mice, they still develop medulloblastomas. Despite nearly normal V(D)J recombination in developing B cells, XLF-deficient mature B cells are moderately defective for immunoglobulin heavy-chain class switch recombination. Together, our results implicate XLF as a C-NHEJ factor but also indicate that developing mouse lymphocytes harbor cell-type-specific factors/pathways that compensate for the absence of XLF function during V(D)J recombination. 相似文献
844.
Rapid development, transparency and small size are the outstanding features of zebrafish that make it as an increasingly important vertebrate system for developmental biology, functional genomics, disease modeling and drug discovery. Zebrafish has been regarded as ideal animal specie for studying the relationship between genotype and phenotype, for pathway analysis and systems biology. However, the tremendous amount of data generated from large numbers of embryos has led to the bottleneck of data analysis and modeling. The zebrafish image quantitator (ZFIQ) software provides streamlined data processing and analysis capability for developmental biology and disease modeling using zebrafish model. AVAILABILITY: ZFIQ is available for download at http://www.cbi-platform.net. 相似文献
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846.
An autonomic provisioning framework for outsourcing data center based on virtual appliances 总被引:1,自引:0,他引:1
Xiaoying Wang Zhihui Du Yinong Chen Sanli Li Dongjun Lan Gang Wang Ying Chen 《Cluster computing》2008,11(3):229-245
As outsourcing data centers emerge to host applications and services from many different organizations, it is critical for
data center owners to isolate different applications while dynamically and optimally allocate sharable resources among them.
To address this issue, we propose a virtual-appliance-based autonomic resource provisioning framework for large virtualized
data centers. We present the architecture of the data center with enriched autonomic features. We define a non-linear constrained
optimization model for dynamic resource provisioning and present a novel analytic solution. Key factors, including virtualization
overhead and reconfiguration delay, are incorporated into the model. Experimental results based on a prototype demonstrate
that the system-level performance has been greatly improved by taking advantage of fine-grained server consolidation, and
the whole system exhibits flexible adaptation in failure scenarios. Experiments with the impact of switching delay also show
the efficiency of the framework due to significantly reduced provisioning time.
相似文献
Zhihui DuEmail: |
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848.
NAD(P)H quinone oxidoreductase 1 inhibits the proteasomal degradation of the tumour suppressor p33(ING1b) 总被引:1,自引:0,他引:1
The tumour suppressor p33(ING1b) ((ING1b) for inhibitor of growth family, member 1b) is important in cellular stress responses, including cell-cycle arrest, apoptosis, chromatin remodelling and DNA repair; however, its degradation pathway is still unknown. Recently, we showed that genotoxic stress induces p33(ING1b) phosphorylation at Ser 126, and abolishment of Ser 126 phosphorylation markedly shortened its half-life. Therefore, we suggest that Ser 126 phosphorylation modulates the interaction of p33(ING1b) with its degradation machinery, stabilizing this protein. Combining the use of inhibitors of the main degradation pathways in the nucleus (proteasome and calpains), partial isolation of the proteasome complex, and in vitro interaction and degradation assays, we set out to determine the degradation mechanism of p33(ING1b). We found that p33(ING1b) is degraded in the 20S proteasome and that NAD(P)H quinone oxidoreductase 1 (NQO1), an oxidoreductase previously shown to modulate the degradation of p53 in the 20S proteasome, inhibits the degradation of p33(ING1b). Furthermore, ultraviolet irradiation induces p33(ING1b) phosphorylation at Ser 126, which, in turn, facilitates its interaction with NQO1. 相似文献
849.
Modifying the DPClus algorithm for identifying protein complexes based on new topological structures 总被引:4,自引:0,他引:4