全文获取类型
收费全文 | 267篇 |
免费 | 32篇 |
出版年
2022年 | 7篇 |
2021年 | 6篇 |
2020年 | 5篇 |
2019年 | 2篇 |
2018年 | 5篇 |
2017年 | 3篇 |
2016年 | 4篇 |
2015年 | 10篇 |
2014年 | 8篇 |
2013年 | 17篇 |
2012年 | 15篇 |
2011年 | 13篇 |
2010年 | 18篇 |
2009年 | 8篇 |
2008年 | 10篇 |
2007年 | 9篇 |
2006年 | 5篇 |
2005年 | 7篇 |
2004年 | 9篇 |
2003年 | 9篇 |
2002年 | 3篇 |
2001年 | 8篇 |
2000年 | 11篇 |
1999年 | 10篇 |
1998年 | 4篇 |
1997年 | 5篇 |
1996年 | 4篇 |
1995年 | 3篇 |
1993年 | 3篇 |
1992年 | 7篇 |
1991年 | 6篇 |
1990年 | 3篇 |
1989年 | 2篇 |
1988年 | 6篇 |
1987年 | 3篇 |
1985年 | 4篇 |
1984年 | 3篇 |
1983年 | 3篇 |
1982年 | 2篇 |
1976年 | 2篇 |
1975年 | 2篇 |
1974年 | 2篇 |
1968年 | 2篇 |
1958年 | 5篇 |
1956年 | 2篇 |
1955年 | 2篇 |
1954年 | 2篇 |
1953年 | 4篇 |
1952年 | 4篇 |
1951年 | 2篇 |
排序方式: 共有299条查询结果,搜索用时 15 毫秒
91.
92.
93.
C S Atwood X Huang A Khatri R C Scarpa Y S Kim R D Moir R E Tanzi A E Roher A I Bush 《Cellular and molecular biology, including cyto-enzymology》2000,46(4):777-783
Abeta derived from amyloid plaques of Alzheimer's disease-affected brain contain several oxidative posttranslational modifications. In this study we have characterized the amino acid content of human amyloid-derived Abeta and compared it with that of human synthetic Abeta subjected to metal-catalyzed oxidation. Human amyloid derived Abeta has an increased content of arginine (46%) and glutamate/glutamine residues (28%), but a decreased content of histidine residues (-32%) as compared to the expected amino acid content. Incubation of synthetic human Abeta with Cu(II), but not Fe(III), in the presence of H2O2 similarly induced a decrease in histidine residues (-79%), but also a decrease in tyrosine residues (-28%). Our results suggest that histidine and tyrosine are most vulnerable to metal mediated oxidative attack, consistent with our earlier findings that Cu coordinated via histidine residues is redox competent. Our results suggest that the loss of histidine residues in human amyloid-derived Abeta may be a result of Cu oxidation, and that unidentified post-translational mechanisms operate to modify other amino acids of Abeta in vivo. 相似文献
94.
Rudolph Tanzi Sandra Gaston Ashley Bush Donna Romano Warren Pettingell Jeffrey Peppercorn Marc Paradis Sarada Gurubhagavatula Barbara Jenkins Wilma Wasco 《Genetica》1993,91(1-3):255-263
Inherited Alzheimer's disease is a genetically heterogeneous disorder that involves gene defects on at least five chromosomal loci. Three of these loci have been found by genetic linkage studies to reside on chromosomes 21, 19, and 14. On chromosomes 21, the gene encoding the precursor protein of Alzheimerassociated amyloid (APP) has been shown to contain several mutations in exons 16 and 17 which account for roughly 2–3% of familial Alzheimer's disease (FAD). The other loci include what appears to be a susceptibility gene on chromosome 19 associated with late-onset (>65 years) FAD, and a major early-onset FAD gene defect on the long arm of chromosome 14. In other early-and late-onset FAD kindreds, the gene defects involved do not appear to be linked to any of these three loci, indicating the existence of additional and as of yet unlocalized FAD genes. This review provides a historical perspective of the search for FAD gene defects and summarizes the progress made in world-wide attempts to isolate and characterize the genes responsible for this disorder. 相似文献
95.
V Taglietti F Tanzi R Romero 《Bollettino della Società italiana di biologia sperimentale》1983,59(7):949-954
Voltage-clamp experiments in full-grown frog oocytes, in a range of membrane potentials from 90 mV negative to 30 mV positive, have revealed the presence of voltage-dependent channels selective for K+, blocked by extracellular TEA. The percentage of open K+-channels increases with membrane depolarizations over a range from -40 mV to +10 mV, thus supporting the outward rectification in the I/V relationship. The current transport through the K+-channels open at different potential levels and in various [K+]o takes place in accordance with the constant-field assumptions. The leakage current of the oocyte membrane was found to be considerable large. 相似文献
96.
97.
Shoot apices of Spinacia oleracea plants have been induced toflower either by: (a) subjecting leaves to 24 h long day, or(b) exposure to a short photoperiod but displaced by 8 h (displacedshort day) in the usual 24 h short-day cycle, or (c) exposureto low temperature (5 °C) during the dark period of thenormal short day. A quantitative cytochemical assay of pentosephosphate pathway activity during floral induction indicatesan approximate doubling of the rate of activity when comparedto that of vegetative apices (short day) (21 °C). Exposure to either low temperature, or a displaced short photoperiodstimulates pentose phosphate pathway activity in the shoot apexin a manner similar to that seen by long-day induction. Thischange in metabolic activity is accompanied by changes in theshape of the shoot apex which resembles that seen at an earlystage during floral induction. Spinacia oleracea, pentose phosphate pathway, shoot apex, glucose-6-phosphate dehydrogenase, floral induction, chilling, displaced short day 相似文献
98.
99.
Hamza Gadhoumi Martinez-Rojas Enriqueta Tounsi Moufida Saidani Hayouni EL Akrem 《Biology Bulletin》2021,48(6):667-672
Biology Bulletin - Erodium glaucophyllum, Erodium hirtum and Erodium guttatum were medicinal herbs from a southern Mediterranean known for its health benefits. There is a strong demand for the find... 相似文献
100.
Polly J Phillips-Mason Sonya EL Craig Susann M Brady-Kalnay 《Cell Adhesion & Migration》2011,5(4):298-305
Dissolution of cell-cell adhesive contacts and increased cell-extracellular matrix adhesion are hallmarks of the migratory and invasive phenotype of cancer cells. These changes are facilitated by growth factor binding to receptor protein tyrosine kinases (RTKs). In normal cells, cell-cell adhesion molecules (CAMs), including some receptor protein tyrosine phosphatases (RPTPs), antagonize RTK signaling by promoting adhesion over migration. In cancer, RTK signaling is constitutive due to mutated or amplified RTKs, which leads to growth factor independence or autonomy. An alternative route for a tumor cell to achieve autonomy is to inactivate cell-cell CAMs such as RPTPs. RPTPs directly mediate cell adhesion and regulate both cadherin-dependent adhesion and signaling. In addition, RPTPs antagonize RTK signaling by dephosphorylating molecules activated following ligand binding. Both RPTPs and cadherins are downregulated in tumor cells by cleavage at the cell surface. This results in shedding of the extracellular, adhesive segment and displacement of the intracellular segment, altering its subcellular localization and access to substrates or binding partners. In this commentary we discuss the signals that are altered following RPTP and cadherin cleavage to promote cell migration. Tumor cells both step on the gas (RTKs) and disconnect the brakes (RPTPs and cadherins) during their invasive and metastatic journey.Key words: receptor protein tyrosine kinase, receptor-like protein tyrosine phosphatase, cadherins, cell adhesion, signal transduction, phospholipase C gamma, protein kinase C, catenins, IQGAP1 protein, regulated intramembrane proteolysis 相似文献