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21.
Crystal structure of an N-terminal fragment of the DNA gyrase B protein. 总被引:22,自引:0,他引:22
The crystal structure of an N-terminal fragment of the Escherichia coli DNA gyrase B protein, complexed with a nonhydrolysable ATP analogue, has been solved at 2.5 A resolution. It consists of two domains, both containing novel protein folds. The protein fragment forms a dimer, whose N-terminal domains are responsible for ATP binding and hydrolysis. The C-terminal domains form the sides of a 20 A hole through the protein dimer which may play a role in DNA strand passage during the supercoiling reaction. 相似文献
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R. A. Maxwell R. P. Mull A. J. Plummer 《Cellular and molecular life sciences : CMLS》1959,15(7):267-267
Résumé On décrit la chimie et la pharmacologie d'un nouvel agent antihypertenseur. 相似文献
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Genetic and structural analyses suggest that a novel SPG3A mutation causes severe phenotypes of hereditary spastic paraplegia 总被引:2,自引:0,他引:2
CHEN Suqin ZHOU Yan LI Xunhua Labu HUANG Shuang HUANG Weijun ZHOU Chunlong MAXWELL Patrick H WANG Yiming 《科学通报(英文版)》2006,51(16):2038-2040
Hereditary spastic paraplegia (HSP) (MIM# 182600, etc.) is a group of heterogeneous neurodegenerative disorders, characterized by lower limb spasticity, hy- perreflexia, progressive spastic gait abnormalities and an extensor-plantar response[1]. The genot… 相似文献
25.
Rivera A Mavila A Bayless KJ Davis GE Maxwell SA 《Cellular and molecular life sciences : CMLS》2006,63(12):1425-1439
We were the first to identify cyclin A1 as a p53-induced gene by cDNA expression profiling of p53-sensitive and -resistant
tumor cells [Maxwell S. A. and Davis G. E. (2000) Proc. Natl. Acad. Sci. USA 97, 13009–13014]. We show here that cyclin A1
can induce G2 cell cycle arrest, polyploidy, apoptosis, and mitotic catastrophe in H1299 non-small cell lung, TOV-21G ovarian,
or 786-0 renal carcinoma cells. More cdk1 protein and kinase activities were observed in cyclin A1-induced cells than in GFP
control-induced cells. Thus, cyclin A1 might mediate apoptosis and mitotic catastrophe through an unscheduled or inappropriate
activation of cdk1. Two primary renal cell carcinomas expressing mutated p53 exhibited reduced or absent expression of cyclin
A1 relative to the corresponding normal tissue. Moreover, renal carcinoma-derived mutant p53s were deficient in inducing cyclin
A1 expression in p53-null cells. Cyclin A1 but not cyclin A2 was upregulated in etoposide-treated tumor cells undergoing p53-dependent
apoptosis and mitotic catastrophe. Forced upregulation of cyclin A2 did not induce apoptosis. The data implicate cyclin A1
as a downstream player in p53-dependent apoptosis and G2 arrest.
Received 1 November 2005; received after revision 17 February 2006; accepted 13 April 2006 相似文献
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Takeda Y Costa S Delamarre E Roncal C Leite de Oliveira R Squadrito ML Finisguerra V Deschoemaeker S Bruyère F Wenes M Hamm A Serneels J Magat J Bhattacharyya T Anisimov A Jordan BF Alitalo K Maxwell P Gallez B Zhuang ZW Saito Y Simons M De Palma M Mazzone M 《Nature》2011,479(7371):122-126
PHD2 serves as an oxygen sensor that rescues blood supply by regulating vessel formation and shape in case of oxygen shortage. However, it is unknown whether PHD2 can influence arteriogenesis. Here we studied the role of PHD2 in collateral artery growth by using hindlimb ischaemia as a model, a process that compensates for the lack of blood flow in case of major arterial occlusion. We show that Phd2 (also known as Egln1) haplodeficient (Phd2(+/-)) mice displayed preformed collateral arteries that preserved limb perfusion and prevented tissue necrosis in ischaemia. Improved arteriogenesis in Phd2(+/-) mice was due to an expansion of tissue-resident, M2-like macrophages and their increased release of arteriogenic factors, leading to enhanced smooth muscle cell (SMC) recruitment and growth. Both chronic and acute deletion of one Phd2 allele in macrophages was sufficient to skew their polarization towards a pro-arteriogenic phenotype. Mechanistically, collateral vessel preconditioning relied on the activation of canonical NF-κB pathway in Phd2(+/-) macrophages. These results unravel how PHD2 regulates arteriogenesis and artery homeostasis by controlling a specific differentiation state in macrophages and suggest new treatment options for ischaemic disorders. 相似文献
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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis. 总被引:123,自引:0,他引:123
P H Maxwell M S Wiesener G W Chang S C Clifford E C Vaux M E Cockman C C Wykoff C W Pugh E R Maher P J Ratcliffe 《Nature》1999,399(6733):271-275
Hypoxia-inducible factor-1 (HIF-1) has a key role in cellular responses to hypoxia, including the regulation of genes involved in energy metabolism, angiogenesis and apoptosis. The alpha subunits of HIF are rapidly degraded by the proteasome under normal conditions, but are stabilized by hypoxia. Cobaltous ions or iron chelators mimic hypoxia, indicating that the stimuli may interact through effects on a ferroprotein oxygen sensor. Here we demonstrate a critical role for the von Hippel-Lindau (VHL) tumour suppressor gene product pVHL in HIF-1 regulation. In VHL-defective cells, HIF alpha-subunits are constitutively stabilized and HIF-1 is activated. Re-expression of pVHL restored oxygen-dependent instability. pVHL and HIF alpha-subunits co-immunoprecipitate, and pVHL is present in the hypoxic HIF-1 DNA-binding complex. In cells exposed to iron chelation or cobaltous ions, HIF-1 is dissociated from pVHL. These findings indicate that the interaction between HIF-1 and pVHL is iron dependent, and that it is necessary for the oxygen-dependent degradation of HIF alpha-subunits. Thus, constitutive HIF-1 activation may underlie the angiogenic phenotype of VHL-associated tumours. The pVHL/HIF-1 interaction provides a new focus for understanding cellular oxygen sensing. 相似文献