全文获取类型
收费全文 | 118篇 |
免费 | 5篇 |
出版年
2020年 | 1篇 |
2018年 | 1篇 |
2017年 | 1篇 |
2014年 | 2篇 |
2013年 | 4篇 |
2012年 | 5篇 |
2011年 | 2篇 |
2008年 | 1篇 |
2007年 | 6篇 |
2006年 | 3篇 |
2005年 | 1篇 |
2004年 | 2篇 |
2003年 | 3篇 |
2001年 | 2篇 |
1992年 | 1篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1980年 | 1篇 |
1979年 | 1篇 |
1977年 | 1篇 |
1973年 | 4篇 |
1972年 | 6篇 |
1971年 | 6篇 |
1970年 | 9篇 |
1969年 | 3篇 |
1968年 | 7篇 |
1967年 | 6篇 |
1966年 | 5篇 |
1965年 | 3篇 |
1964年 | 4篇 |
1963年 | 3篇 |
1962年 | 5篇 |
1961年 | 4篇 |
1960年 | 4篇 |
1959年 | 3篇 |
1958年 | 2篇 |
1956年 | 4篇 |
1955年 | 5篇 |
排序方式: 共有123条查询结果,搜索用时 15 毫秒
31.
From a sample of 122 natural isolates of Neurospora intermedia collected recently from around the world, five variants had erratic stop-start growth patterns reminiscent of the phenotype of "stopper" laboratory extranuclear mutants of Neurospora crassa. Like laboratory isolated mutants, the natural "stopper" variants were sterile as protoperithecial parents and transmitted the variant growth phenotypes very inefficiently, if at all, as male parents. Heterokaryon tests could not be made because of strain incompatibilities. Four of the variants have mitochondrial cytochrome aa3 and b deficiencies. These four variants are all defective in mitochondrial ribosome assembly and have abnormal ratios of large to small subunits. Restriction enzyme analyses revealed some similarity of N. intermedia to N. crassa mtDNA. One normal and four variant strains had additional DNA in comparison to a standard normal strain. Cumulatively, the results indicate that the genetic alterations which cause stopper phenotypes of these natural isolates of N. intermedia are of mitochondrial rather than nuclear origin. 相似文献
32.
Mendheim Müller-Using Nüsslein Rieck v. Xylander 《European Journal of Wildlife Research》1959,5(4):113-120
33.
34.
35.
Monika Ehling-Schulz Martina Fricker Harald Grallert Petra Rieck Martin Wagner Siegfried Scherer 《BMC microbiology》2006,6(1):20-11
Background
Cereulide, a depsipeptide structurally related to valinomycin, is responsible for the emetic type of gastrointestinal disease caused by Bacillus cereus. Recently, it has been shown that this toxin is produced by a nonribosomal peptide synthetase (NRPS), but its exact genetic organization and biochemical synthesis is unknown. 相似文献36.
Blanchard V Liu X Eigel S Kaup M Rieck S Janciauskiene S Sandig V Marx U Walden P Tauber R Berger M 《Biotechnology and bioengineering》2011,108(9):2118-2128
Human alpha‐1‐antitrypsin (A1AT) is a protease inhibitor that is involved in the protection of lungs from neutrophil elastase enzyme that drastically modifies tissue functioning. The glycoprotein consists of 394 amino acids and is N‐glycosylated at Asn‐46, Asn‐83, and Asn‐247. A1AT deficiency is currently treated with A1AT that is purified from human serum. In view of therapeutic applications, rA1AT was produced using a novel human neuronal cell line (AGE1.HN®) and we investigated the N‐glycosylation pattern as well as the in vitro anti‐inflammatory activity of the recombinant glycoprotein. rA1AT (300 mg/L) was biologically active as analyzed using elastase assay. The N‐glycan pool, released by PNGase F digestion, was characterized using 2D‐HPLC, MALDI‐TOF mass spectrometry, and by exoglycosidase digestions. A total of 28 N‐glycan structures were identified, ranging from diantennary to tetraantennary complex‐type N‐glycans. Most of the N‐glycans were found to be (α1–6) core‐fucosylated and part of them contain the Lewis X epitope. The two major compounds are a monosialylated diantennary difucosylated glycan and a disialylated diantennary core‐fucosylated glycan, representing 25% and 18% of the total N‐glycan pool, respectively. Analysis of the site‐specificity revealed that Asn‐247 was mainly occupied by diantennary N‐glycans whereas Asn‐46 was occupied by di‐, and triantennary N‐glycans. Asn‐83 was exclusively occupied by sialylated tri‐ and tetraantennary N‐glycans. Next, we evaluated the anti‐inflammatory activity of rA1AT using A1AT purified from human serum as a reference. rA1AT was found to inhibit the production of TNF‐α in neutrophils and monocytes as commercial A1AT does. Biotechnol. Bioeng. 2011;108:2118–2128. © 2011 Wiley Periodicals, Inc. 相似文献
37.
Habib T Funk A Rieck M Brahmandam A Dai X Panigrahi AK Luning Prak ET Meyer-Bahlburg A Sanda S Greenbaum C Rawlings DJ Buckner JH 《Journal of immunology (Baltimore, Md. : 1950)》2012,188(1):487-496
The PTPN22 genetic variant 1858T, encoding Lyp620W, is associated with multiple autoimmune disorders for which the production of autoantibodies is a common feature, suggesting a loss of B cell tolerance. Lyp620W results in blunted BCR signaling in memory B cells. Because BCR signal strength is tightly coupled to central and peripheral tolerance, we examined whether Lyp620W impacts peripheral B cell homeostasis in healthy individuals heterozygous for the PTPN221858T variant. We found that these subjects display alterations in the composition of the B cell pool that include specific expansion of the transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets. The PTPN22 1858T variant was further associated with significantly diminished BCR signaling and a resistance to apoptosis in both transitional and naive B cells. Strikingly, parallel changes in both BCR signaling and composition of B cell compartment were observed in type 1 diabetic subjects, irrespective of PTPN22 genotype, revealing a novel immune phenotype and likely shared mechanisms leading to a loss of B cell tolerance. Our combined findings suggest that Lyp620W-mediated effects, due in part to the altered BCR signaling threshold, contribute to breakdown of peripheral tolerance and the entry of autoreactive B cells into the naive B cell compartment. 相似文献
38.
39.
40.