排序方式: 共有16条查询结果,搜索用时 31 毫秒
1.
Simons Pickhan Englmann A. Laqueur Halberstädter Alb Simons Zuppinger E. Goldberger Walther Hannes 《Journal of cancer research and clinical oncology》1931,34(5):196-208
Ohne Zusammenfassung 相似文献
2.
A. Simons Fritz Händel Langendorff Josef Frank F. Eillinger Happel Zwerg Fried Walter Schaefer Hedfeld E. Philipp Wehefritz Englmann 《Journal of cancer research and clinical oncology》1932,36(5-6):125-128
Ohne Zusammenfassung 相似文献
3.
4.
Küster Haagen Englmann V. E. Mertens Tannenberg F. Starlinger E. Philipp A. Brunner Stephan Epstein 《Journal of cancer research and clinical oncology》1932,36(2-3):34-35
Ohne Zusammenfassung 相似文献
5.
Schlossarek S Englmann DR Sultan KR Sauer M Eschenhagen T Carrier L 《Basic research in cardiology》2012,107(1):235
Several lines of evidence suggest that alterations of the ubiquitin-proteasome system (UPS) and autophagy-lysosome pathway
(ALP) may be involved in cardiac diseases. Little is known, however, in hypertrophic cardiomyopathy (HCM). This study studied
these pathways in two mouse models of HCM that mainly differ by the presence or absence of truncated mutant proteins. Analyses
were performed in homozygous Mybpc3-targeted knock-in (KI) mice, carrying a HCM mutation and exhibiting low levels of mutant cardiac myosin-binding protein C
(cMyBP-C), and in Mybpc3-targeted knock-out (KO) mice expressing no cMyBP-C, thus serving as a model of pure cMyBP-C insufficiency. In the early postnatal
development of cardiac hypertrophy, both models showed higher levels of ubiquitinated proteins and greater proteasomal activities.
To specifically monitor the degradation capacity of the UPS with age, mice were crossed with transgenic mice that overexpress
UbG76V-GFP. UbG76V-GFP protein levels were fourfold higher in 1-year-old KI, but not KO mice, suggesting a specific UPS impairment in mice expressing
truncated cMyBP-C. Whereas protein levels of key ALP markers were higher, suggesting ALP activation in both mutant mice, their
mRNA levels did not differ between the groups, underlying rather defective ALP-mediated degradation. Analysis of key proteins
regulated in heart failure did not reveal specific alterations in KI and KO mice. Our data suggest (1) UPS activation in early
postnatal development of cardiac hypertrophy, (2) specific UPS impairment in old KI mice carrying a HCM mutation, and (3)
defective ALP as a common mechanism in genetically engineered mice with cardiac hypertrophy. 相似文献
6.
7.
The relation of cognitive load and pupillary unrest 总被引:1,自引:0,他引:1
Müller A Petru R Seitz L Englmann I Angerer P 《International archives of occupational and environmental health》2011,84(5):561-567
Objective
This study examines the relationship between pupillary unrest (PU) and cognitive load. 相似文献8.
O. Noga C. Englmann G. Hanf A. Grützkau J. Seybold G. Kunkel 《Clinical and experimental allergy》2003,33(5):649-654
9.
10.