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排序方式: 共有79条查询结果,搜索用时 437 毫秒
61.
Chan VS Chan KY Chen Y Poon LL Cheung AN Zheng B Chan KH Mak W Ngan HY Xu X Screaton G Tam PK Austyn JM Chan LC Yip SP Peiris M Khoo US Lin CL 《Nature genetics》2006,38(1):38-46
Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection. 相似文献
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APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy 总被引:24,自引:0,他引:24
Rovelet-Lecrux A Hannequin D Raux G Le Meur N Laquerrière A Vital A Dumanchin C Feuillette S Brice A Vercelletto M Dubas F Frebourg T Campion D 《Nature genetics》2006,38(1):24-26
We report duplication of the APP locus on chromosome 21 in five families with autosomal dominant early-onset Alzheimer disease (ADEOAD) and cerebral amyloid angiopathy (CAA). Among these families, the duplicated segments had a minimal size ranging from 0.58 to 6.37 Mb. Brains from individuals with APP duplication showed abundant parenchymal and vascular deposits of amyloid-beta peptides. Duplication of the APP locus, resulting in accumulation of amyloid-beta peptides, causes ADEOAD with CAA. 相似文献
63.
Karnoub AE Dash AB Vo AP Sullivan A Brooks MW Bell GW Richardson AL Polyak K Tubo R Weinberg RA 《Nature》2007,449(7162):557-563
Mesenchymal stem cells have been recently described to localize to breast carcinomas, where they integrate into the tumour-associated stroma. However, the involvement of mesenchymal stem cells (or their derivatives) in tumour pathophysiology has not been addressed. Here, we demonstrate that bone-marrow-derived human mesenchymal stem cells, when mixed with otherwise weakly metastatic human breast carcinoma cells, cause the cancer cells to increase their metastatic potency greatly when this cell mixture is introduced into a subcutaneous site and allowed to form a tumour xenograft. The breast cancer cells stimulate de novo secretion of the chemokine CCL5 (also called RANTES) from mesenchymal stem cells, which then acts in a paracrine fashion on the cancer cells to enhance their motility, invasion and metastasis. This enhanced metastatic ability is reversible and is dependent on CCL5 signalling through the chemokine receptor CCR5. Collectively, these data demonstrate that the tumour microenvironment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells. 相似文献
64.
Wang K Kan J Yuen ST Shi ST Chu KM Law S Chan TL Kan Z Chan AS Tsui WY Lee SP Ho SL Chan AK Cheng GH Roberts PC Rejto PA Gibson NW Pocalyko DJ Mao M Xu J Leung SY 《Nature genetics》2011,43(12):1219-1223
Gastric cancer is a heterogeneous disease with multiple environmental etiologies and alternative pathways of carcinogenesis. Beyond mutations in TP53, alterations in other genes or pathways account for only small subsets of the disease. We performed exome sequencing of 22 gastric cancer samples and identified previously unreported mutated genes and pathway alterations; in particular, we found genes involved in chromatin modification to be commonly mutated. A downstream validation study confirmed frequent inactivating mutations or protein deficiency of ARID1A, which encodes a member of the SWI-SNF chromatin remodeling family, in 83% of gastric cancers with microsatellite instability (MSI), 73% of those with Epstein-Barr virus (EBV) infection and 11% of those that were not infected with EBV and microsatellite stable (MSS). The mutation spectrum for ARID1A differs between molecular subtypes of gastric cancer, and mutation prevalence is negatively associated with mutations in TP53. Clinically, ARID1A alterations were associated with better prognosis in a stage-independent manner. These results reveal the genomic landscape, and highlight the importance of chromatin remodeling, in the molecular taxonomy of gastric cancer. 相似文献
65.
Annie B. Elliott 《Cellular and molecular life sciences : CMLS》1968,24(6):557-558
Résumé En employant des crapauds pour doser l'action des peptides sur la perméabilité de la peau, l'effet hydrosmotique de l'arginine8-vasotocine s'est montré 200 fois plus puissant que celui de l'ornithine8-oxytocine. Ce fait confirme l'importance hydrosmotique de l'acide aminé arginine dans la position 8. Tous 2 ont eu un effet natriférique, mais ce ne fut pas le cas de la lysine8-vasopressine et l'ornithine8-vasopressine. L'importance natriférique de l'acide aminé isoleucine dans la position 3 en est confirmée. 相似文献
66.
Morin R. D. Benington F. Mitchell S. R. Beaton J. M. Bradley R. J. Smythies J. R. 《Cellular and molecular life sciences : CMLS》1975,31(1):93-95
Cellular and Molecular Life Sciences - Le comportement des rats a été fortement influencé par des dérivés de la 2,5-diméthoxyamphétamine Le mécanisme... 相似文献
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Huber C Dias-Santagata D Glaser A O'Sullivan J Brauner R Wu K Xu X Pearce K Wang R Uzielli ML Dagoneau N Chemaitilly W Superti-Furga A Dos Santos H Mégarbané A Morin G Gillessen-Kaesbach G Hennekam R Van der Burgt I Black GC Clayton PE Read A Le Merrer M Scambler PJ Munnich A Pan ZQ Winter R Cormier-Daire V 《Nature genetics》2005,37(10):1119-1124
Intrauterine growth retardation is caused by maternal, fetal or placental factors that result in impaired endovascular trophoblast invasion and reduced placental perfusion. Although various causes of intrauterine growth retardation have been identified, most cases remain unexplained. Studying 29 families with 3-M syndrome (OMIM 273750), an autosomal recessive condition characterized by severe pre- and postnatal growth retardation, we first mapped the underlying gene to chromosome 6p21.1 and then identified 25 distinct mutations in the gene cullin 7 (CUL7). CUL7 assembles an E3 ubiquitin ligase complex containing Skp1, Fbx29 (also called Fbw8) and ROC1 and promotes ubiquitination. Using deletion analysis, we found that CUL7 uses its central region to interact with the Skp1-Fbx29 heterodimer. Functional studies indicated that the 3-M-associated CUL7 nonsense and missense mutations R1445X and H1464P, respectively, render CUL7 deficient in recruiting ROC1. These results suggest that impaired ubiquitination may have a role in the pathogenesis of intrauterine growth retardation in humans. 相似文献