排序方式: 共有32条查询结果,搜索用时 203 毫秒
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Marian Johnston 《Cellular and molecular life sciences : CMLS》1967,23(2):152-154
Zusammenfassung Die Geschwindigkeit der Histaminbildung wurde bei Ratten von experimentellem Walker Carcinosarcom kontrolliert. Bei Parabiosen konnte gezeigt werden, dass der Faktor, welcher diese Histaminbildung auslöst, mit dem Blutstrom übertragen wird.
This study was supported by U.S. Public Health Service grant No. 5RO1 HDOO255-06 to Prof.G. Kahlson, whose interest is gratefully acknowledged. Merck, Sharp and Dohme, Rahway, N.J., USA, kindly gave the -methylhistidine. 相似文献
This study was supported by U.S. Public Health Service grant No. 5RO1 HDOO255-06 to Prof.G. Kahlson, whose interest is gratefully acknowledged. Merck, Sharp and Dohme, Rahway, N.J., USA, kindly gave the -methylhistidine. 相似文献
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Regulation of progenitor cell proliferation and granulocyte function by microRNA-223 总被引:1,自引:0,他引:1
Johnnidis JB Harris MH Wheeler RT Stehling-Sun S Lam MH Kirak O Brummelkamp TR Fleming MD Camargo FD 《Nature》2008,451(7182):1125-1129
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The authors present the main ideas of the computer-assisted proof of Mischaikow and Mrozek that chaos is really present in the Lorenz equations. Methodological consequences of this proof are examined. It is shown that numerical calculations can constitute an essential part of mathematical proof not only in the discrete mathematics but also in the mathematics of continua. 相似文献
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Serena Stadler Chi Huu Nguyen Helga Schachner Daniela Milovanovic Silvio Holzner Stefan Brenner Julia Eichsteininger Mira Stadler Daniel Senfter Liselotte Krenn Wolfgang M. Schmidt Nicole Huttary Sigurd Krieger Oskar Koperek Zsuzsanna Bago-Horvath Konstantin Alexander Brendel Brigitte Marian Oliver de Wever Robert M. Mader Benedikt Giessrigl Walter Jäger Helmut Dolznig Georg Krupitza 《Cellular and molecular life sciences : CMLS》2017,74(10):1907-1921
Retraction of mesenchymal stromal cells supports the invasion of colorectal cancer cells (CRC) into the adjacent compartment. CRC-secreted 12(S)-HETE enhances the retraction of cancer-associated fibroblasts (CAFs) and therefore, 12(S)-HETE may enforce invasivity of CRC. Understanding the mechanisms of metastatic CRC is crucial for successful intervention. Therefore, we studied pro-invasive contributions of stromal cells in physiologically relevant three-dimensional in vitro assays consisting of CRC spheroids, CAFs, extracellular matrix and endothelial cells, as well as in reductionist models. In order to elucidate how CAFs support CRC invasion, tumour spheroid-induced CAF retraction and free intracellular Ca2+ levels were measured and pharmacological- or siRNA-based inhibition of selected signalling cascades was performed. CRC spheroids caused the retraction of CAFs, generating entry gates in the adjacent surrogate stroma. The responsible trigger factor 12(S)-HETE provoked a signal, which was transduced by PLC, IP3, free intracellular Ca2+, Ca2+-calmodulin-kinase-II, RHO/ROCK and MYLK which led to the activation of myosin light chain 2, and subsequent CAF mobility. RHO activity was observed downstream as well as upstream of Ca2+ release. Thus, Ca2+ signalling served as central signal amplifier. Treatment with the FDA-approved drugs carbamazepine, cinnarizine, nifedipine and bepridil HCl, which reportedly interfere with cellular calcium availability, inhibited CAF-retraction. The elucidation of signalling pathways and identification of approved inhibitory drugs warrant development of intervention strategies targeting tumour–stroma interaction. 相似文献
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P. F. Han Y. H. Marian H. W. Matthews J. Johnson 《Cellular and molecular life sciences : CMLS》1981,37(7):687-689
Summary Yeast glucose-6-P dehydrogenase is irreversibly inactivated by penicillin G. Kinetic data show that 1 molecule of penicillin G reacts with each active unit when the enzyme is inactivated The rate of inactivation increases greatly with increasing pH. This irreversible inactivation by penicillin G is largely prevented by pyridoxal-P, a reversible inactivator of this enzyme. Prior treatment of penicillin G with penicillinase totally abolishes its ability to inactivate the enzyme.This work was supported by grant RR-8006 from the General Research Branch, Division of Research Resouces, NIH (USA). 相似文献
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Cichon S Buervenich S Kirov G Akula N Dimitrova A Green E Schumacher J Klopp N Becker T Ohlraun S Schulze TG Tullius M Gross MM Jones L Krastev S Nikolov I Hamshere M Jones I Czerski PM Leszczynska-Rodziewicz A Kapelski P Bogaert AV Illig T Hauser J Maier W Berrettini W Byerley W Coryell W Gershon ES Kelsoe JR McInnis MG Murphy DL Nurnberger JI Reich T Scheftner W O'Donovan MC Propping P Owen MJ Rietschel M Nöthen MM McMahon FJ Craddock N 《Nature genetics》2004,36(8):783-4; author reply 784-5
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Sirajuddin M Farkasovsky M Hauer F Kühlmann D Macara IG Weyand M Stark H Wittinghofer A 《Nature》2007,449(7160):311-315
Septins are GTP-binding proteins that assemble into homo- and hetero-oligomers and filaments. Although they have key roles in various cellular processes, little is known concerning the structure of septin subunits or the organization and polarity of septin complexes. Here we present the structures of the human SEPT2 G domain and the heterotrimeric human SEPT2-SEPT6-SEPT7 complex. The structures reveal a universal bipolar polymer building block, composed of an extended G domain, which forms oligomers and filaments by conserved interactions between adjacent nucleotide-binding sites and/or the amino- and carboxy-terminal extensions. Unexpectedly, X-ray crystallography and electron microscopy showed that the predicted coiled coils are not involved in or required for complex and/or filament formation. The asymmetrical heterotrimers associate head-to-head to form a hexameric unit that is nonpolarized along the filament axis but is rotationally asymmetrical. The architecture of septin filaments differs fundamentally from that of other cytoskeletal structures. 相似文献
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