全文获取类型
收费全文 | 180篇 |
免费 | 15篇 |
专业分类
195篇 |
出版年
2022年 | 2篇 |
2021年 | 4篇 |
2020年 | 2篇 |
2019年 | 2篇 |
2018年 | 6篇 |
2017年 | 4篇 |
2016年 | 3篇 |
2015年 | 7篇 |
2014年 | 10篇 |
2013年 | 10篇 |
2012年 | 6篇 |
2011年 | 8篇 |
2010年 | 5篇 |
2009年 | 7篇 |
2008年 | 5篇 |
2007年 | 9篇 |
2006年 | 11篇 |
2005年 | 10篇 |
2004年 | 7篇 |
2003年 | 6篇 |
2002年 | 2篇 |
2001年 | 5篇 |
2000年 | 3篇 |
1999年 | 3篇 |
1998年 | 2篇 |
1997年 | 2篇 |
1996年 | 2篇 |
1995年 | 2篇 |
1994年 | 1篇 |
1992年 | 2篇 |
1991年 | 1篇 |
1987年 | 1篇 |
1986年 | 6篇 |
1985年 | 7篇 |
1984年 | 6篇 |
1983年 | 7篇 |
1982年 | 3篇 |
1981年 | 4篇 |
1980年 | 3篇 |
1976年 | 1篇 |
1974年 | 1篇 |
1969年 | 5篇 |
1963年 | 1篇 |
1961年 | 1篇 |
排序方式: 共有195条查询结果,搜索用时 9 毫秒
161.
Hyaluronate lyase activity of staphylococci 总被引:1,自引:0,他引:1
162.
Ashim C. Roy Wu-Xiang Liao Ying Chen Sabaratnam Arulkumaran Shan S. Ratnam 《Molecular and cellular biochemistry》1996,165(2):151-153
Seven new point mutations have been identified from LH -subunit gene by PCR-mediated SSCP, and sequencing. One mutation was found changing amino acid from Gln102 to Ser102. The remaining six mutations, which did not change the codings, were in complete linkage disequilibrium. SSCP can be used in the diagnosis of LH-related disorders. 相似文献
163.
164.
Regulation of Notch signalling by non-visual beta-arrestin 总被引:1,自引:0,他引:1
Mukherjee A Veraksa A Bauer A Rosse C Camonis J Artavanis-Tsakonas S 《Nature cell biology》2005,7(12):1191-1201
Signalling activity of the Notch receptor, which plays a fundamental role in metazoan cell fate determination, is controlled at multiple levels. We uncovered a Notch signal-controlling mechanism that depends on the ability of the non-visual beta-arrestin, Kurtz (Krz), to influence the degradation and, consequently, the function of the Notch receptor. We identified Krz as a binding partner of a known Notch-pathway modulator, Deltex (Dx), and demonstrated the existence of a trimeric Notch-Dx-Krz protein complex. This complex mediates the degradation of the Notch receptor through a ubiquitination-dependent pathway. Our results establish a novel mode of regulation of Notch signalling and define a new function for non-visual beta-arrestins. 相似文献
165.
Kerkar N Choudhuri K Ma Y Mahmoud A Bogdanos DP Muratori L Bianchi F Williams R Mieli-Vergani G Vergani D 《Journal of immunology (Baltimore, Md. : 1950)》2003,170(3):1481-1489
Cytochrome P4502D6 (CYP2D6), target of liver kidney microsomal autoantibody type 1 (LKM1), characterizes autoimmune hepatitis type 2 (AIH2) but is also found in patients with chronic hepatitis C virus (HCV) infection. To provide a complete linear epitope B cell map of CYP2D6, we tested peptides spanning the entire sequence of CYP2D6. In addition to confirming previously described antigenic sites, we identified four new epitopes (193-212, 238-257, 268-287, and 478-497). CYP2D6(193-212) is immunodominant and was the target of 12 of 13 (93%) patients with AIH2 and 5 of 10 (50%) HCV/LKM1-positive patients. Because LKM1 is present in both AIH2 and a viral infection, we tested whether Abs to CYP2D6(193-212) arise through cross-reactive immunity between virus and self. We identified a hexameric sequence "RLLDLA" sharing 5 of 6 aa with "RLLDLS" of HCV(2985-2990) and all 6 aa with CMV(130-135). Of 17 CYP2D6(193-212)-reactive sera, 11 (7 AIH and 4 HCV) reacted by ELISA with the HCV homologue, 8 (5 AIH and 3 HCV) with the CMV homologue, and 8 (5 AIH and 3 HCV) showed double reactivity. Autoantibody binding to CYP2D6(193-212) was inhibited by preincubation with HCV(2977-2996) or CMV(121-140). Recombinant HCV-nonstructural protein 5 and CMV-UL98 proteins also inhibited Ab binding to CYP2D6(193-212). Affinity-purified CYP2D6(193-212)-specific Ab inhibited the metabolic activity of CYP2D6. The demonstrated similarity and cross-reactivity between CYP2D6(193-212) and two unrelated viruses suggests that multiple exposure to viruses mimicking self may represent an important pathway to the development of autoimmunity. 相似文献
166.
167.
168.
Supratim Choudhuri 《Journal of biochemical and molecular toxicology》2010,24(3):195-216
In recent years, the discovery of small ncRNAs (noncoding RNAs) has unveiled a slew of powerful riboregulators of gene expression. So far, many different types of small ncRNAs have been described. Of these, miRNAs (microRNAs), siRNAs (small interfering RNAs), and piRNAs (Piwi‐interacting RNAs) have been studied in more detail. A significant fraction of genes in most organisms and tissues is targets of these small ncRNAs. Because these tiny RNAs are turning out to be important regulators of gene and genome expression, their aberrant expression profiles are expected to be associated with cellular dysfunction and disease. In fact, an ever‐increasing number of studies have implicated miRNAs and siRNAs in human health and disease ranging from metabolic disorders to diseases of various organ systems as well as various forms of cancer. Nevertheless, despite the flurry of research on these small ncRNAs, many aspects of their biology still remain to be understood. The following discussion focuses on some aspects of the biogenesis and function of small ncRNAs with major emphasis on miRNAs since these are the most widespread endogenous small ncRNAs that have been called “micromanagers” of gene expression. Their emerging significance in toxicology is also discussed. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:195–216, 2010; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20325 相似文献
169.
One of the important pathways of resistance to anthracyclines is governed by elevated levels of glutathione (GSH) in cancer cells. Resistant cells having elevated levels of GSH show higher expression of multidrug-resistant protein (MRP); the activity of glutathione S-transferases (GSTs) group of enzymes have also been found to be higher in some drug-resistant cells. The general mechanism in this type of resistance seems to be the formation of conjugates enzymatically by GSTs, and subsequent efflux by active transport through MRP (MRP1-MRP9). MRPs act as drug efflux pump and can also co-transport drugs like doxorubicin (Dox) with GSH. Depletion of GSH in resistant neoplastic cells may possibly sensitize such cells, and thus overcome multidrug resistance (MDR). A number of resistance modifying agents (RMA) like DL-buthionine (S, R) sulfoxamine (BSO) and ethacrynic acid (EA) moderately modulate resistance by acting as a GSH-depleting agent. As most of the GSH-depleting agents have dose-related toxicity, development of non-toxic GSH-depleting agent has immense importance in overcoming MDR. The present study describes the resistance reversal potentiality of novel copper complex, viz., copper N-(2-hydroxy acetophenone) glycinate (CuNG) developed by us in Dox-resistant Ehrlich ascites carcinoma (EAC/Dox) cells. CuNG depletes GSH in resistant (EAC/Dox) cells possibly by forming conjugate with it. Depletion of GSH results in higher Dox accumulation that may lead to enhanced rate of apoptosis in EAC/Dox cells. In vivo studies with male Swiss albino mice bearing ascitic growth of EAC/Dox showed tremendous increase in life span (treated/control, T/C = 453%) for the treated group with apparent regression of tumor. Resistance to Dox in EAC/Dox cells is associated with over expression of GST-P1, GST-M1 (enzymes involved in phase II detoxification) and MRP1 (a transmembrane ATPase efflux pump for monoglutathionyl conjugates of xenobiotics). CuNG causes down regulation of all these three proteins in EAC/Dox cells. The effect of CuNG as RMA is better than BSO in many aspects. 相似文献
170.