全文获取类型
收费全文 | 319篇 |
免费 | 13篇 |
出版年
2023年 | 1篇 |
2022年 | 3篇 |
2021年 | 10篇 |
2020年 | 3篇 |
2019年 | 4篇 |
2018年 | 8篇 |
2017年 | 6篇 |
2016年 | 14篇 |
2015年 | 14篇 |
2014年 | 15篇 |
2013年 | 20篇 |
2012年 | 23篇 |
2011年 | 35篇 |
2010年 | 10篇 |
2009年 | 12篇 |
2008年 | 13篇 |
2007年 | 23篇 |
2006年 | 21篇 |
2005年 | 12篇 |
2004年 | 12篇 |
2003年 | 18篇 |
2002年 | 9篇 |
2001年 | 5篇 |
2000年 | 1篇 |
1999年 | 5篇 |
1998年 | 2篇 |
1997年 | 5篇 |
1996年 | 2篇 |
1995年 | 2篇 |
1994年 | 2篇 |
1993年 | 2篇 |
1992年 | 5篇 |
1991年 | 4篇 |
1990年 | 1篇 |
1988年 | 3篇 |
1987年 | 1篇 |
1986年 | 1篇 |
1985年 | 1篇 |
1984年 | 2篇 |
1980年 | 1篇 |
1977年 | 1篇 |
排序方式: 共有332条查询结果,搜索用时 15 毫秒
1.
2.
Indu S. Ambudkar Timothy Lockwich Yukiharu Hiramatsu Bruce J. Baum 《Molecular and cellular biochemistry》1992,114(1-2):73-77
Conclusions While it is generally accepted that Ca2+ plays an important regulatory role in the physiology of a number of non-excitable cells, the mechanisms which regulate intracellular [Ca2+ are far from well established. Ca2+ transporting mechanisms which distribute Ca2+ intracellularly as well as those which allow influx of extracellular Ca2+ are involved in mediating intracellular Ca2+ homestasis. In this paper we have described recent studies on the regulation of the Ca2+ influx system in the data, it appears that the process of Ca2+ entry is extremely complex and may involve several levels of regulation. Understanding the molecular basis of these regulatory mechanisms presents a challeging problem for future studies. 相似文献
3.
Valerie J. Horn Paul A. Sheehy Miriam B. Goodman Indu S. Ambudkar 《Molecular and cellular biochemistry》1991,101(1):43-49
Intracellular Ca2+ mobilization events were assessed in mouse L cells, which contain native prostaglandin E1 receptors and transfected human 2 adrenergic receptors. Both Fura2 (single cell measurements) and Quin 2, (cuvette assays) were used to determine [Ca2+]i levels. Our results demonstrate that in the transfected cells there is a dose-dependent increase in [Ca2+]i in response to isoproterenol (0.1 nM–100 nM), which is inhibited by the -adrenergic antagonist, propranolol, and is a result of intracellular Ca2+ release. [Ca2+]1 in these cells was also increased by prostaglandin E1, 8 bromo cyclic AMP, and aluminum fluoride. Both 8 bromo cAMP and isoproterenol induced a rapid increase in the levels of IP1, IP2, and IP3. The data presented demonstrate that the elevation of intracellular cyclic AMP induces an increase in IP3 production which leads to an elevation in [Ca2+];. We propose that this cyclic AMP dependent activation of the IP3 generating system occurs at a post-receptor site.Abbreviations cAMP
Adenosine Cyclic 3-5-Monophosphate
- [Ca2+]i
intracellular [Ca2+]i
- 8 Br cAMP
8 Bromo Adenosine Cyclic 3-5-Monophosphate
- DAG
Diacylglycerol
- EGTA]
[Ethylene Bis (oxyethylenenitrilo)] Tetracetic acid
- BSA
Bovine Serum Albumin
- HBSS-H
Hanks' Balanced Salt Solution buffered with HEPES to pH 7.4
- HEPES
4-(2-Hydroxyethyl)-1-piperazineethanesulfonic acid
- PIP2
Phosphatidylinositol 4,5-bisphosphate
- IP2
Inositol 4 Phosphate
- IP2
Inositol 4,5 Bisphosphate
- IP3
Inositol Trisphosphate
- PGE1
Prostaglandin E1
- PBS
Phosphate Buffered Saline Solution 相似文献
4.
Yukiharu Hiramatsu Indu S. Ambudkar Bruce J. Baum 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1991,1092(3):391-396
β-Adrenergic receptor stimulation of adenylyl cyclase involves the activation of a GTP-binding regulatory protein (G-protein, termed here Gs). Inactivation of this G-protein is associated with the hydrolysis of bound GTP by an intrinsic high affinity GTPase activity. In the present study, we have characterized the GTPase activity in a Gs-enriched rat parotid gland membrane fraction. Two GTPase activities were resolved; a high affinity GTPase activity displaying Michaelis-Menten kinetics with increasing concentrations of GTP, and a low affinity GTPase activity which increased linearly with GTP concentrations up to 10 mM. The β-adrenergic agonist isoproterenol (10 μM) increased the Vmax of the high affinity GTPase component approx. 50% from 90 to 140 pmol/mg protein per min, but did not change its Km value (≈ 450 nM). Isoproterenol also stimulated adenylyl cyclase activity in parotid membranes both in the absence or presence of GTP. In the presence of a non-hydrolyzable GTP analogue, guanosine 5′-(3-O-thio)triphosphate (GTPγS), isoproterenol increased cAMP formation to the same extent as that observed with AlF4?. Cholera toxin treatment of parotid membranes led to the ADP-ribosylation of two proteins (≈ 45 and 51 kDa). Cholera toxin also specifically decreased the high affinity GTPase activity in membranes and increased cAMP formation induced by GTP in the absence or the presence of isoproterenol. These data demonstrate that the high affinity GTPase characterized here is the ‘turn-off’ step for the adenylyl cyclase activation seen following β-adrenergic stimulation of rat parotid glands. 相似文献
5.
6.
7.
Anil K. Mantha Indu R. Chandrashekar Najma Z. Baquer Sudha M. Cowsik 《Journal of biomolecular structure & dynamics》2013,31(2):137-147
Abstract Neurokinin B (NKB), a decapeptide of mammalian origin exhibits a variety of biological activities such as regulatory functions in reproduction, pre-eclampsia and neuroprotection in Alzheimer's disease. In order to gain insight into structure-function relationship, three- dimensional structure of NKB has been investigated using CD spectropolarimetry and two-dimensional proton nuclear magnetic resonance (2D 1H-NMR) spectroscopy in aqueous and membrane mimetic solvents. Unambiguous NMR assignments of resonances have been made with the aid of correlation spectroscopy (DQF-COSY and TOCSY) experiments and Nuclear Overhauser Effect Spectroscopy (NOESY) experiments. Distance constraints obtained from the NMR data have been used to generate a family of structures, which have been refined using restrained energy minimization and dynamics. Our data show that a helical structure is induced in NKB, in presence of perdeuterated dodecyl phosphocholine (DPC) micelles, a membrane model system. Further, the conformation adopted by NKB in presence of DPC micelles represents a structural motif typical of neurokinin-3 selective agonists. 相似文献
8.
Antoaneta B. M. Kroumova Dipak K. Sahoo Sumita Raha Michael Goodin Indu B. Maiti George J. Wagner 《Plant cell reports》2013,32(11):1771-1782
Key message
Phylloplanins are plant-derived, antifungal glycoproteins produced by leaf trichomes. Expression of phylloplanin-GFP fusion gene to the apoplast of a blue mold susceptible tobacco resulted in increased resistance to this pathogen.Abstract
Tobaccos and certain other plants secrete phylloplanin glycoproteins to aerial surfaces where they appear to provide first-point-of-contact resistance against fungi/fungi-like pathogens. These proteins can be collected by water washing of aerial plant surfaces, and as shown for tobacco and a sunflower phylloplanins, spraying concentrated washes onto, e.g., turf grass aerial surfaces can provide resistance against various fungi/fungi-like pathogens, in the laboratory. These results suggest that natural-product, phylloplanins may be useful as broad-selectivity fungicides. An obvious question now is can a tobacco phylloplanin gene be introduced into a disease-susceptible plant to confer endogenous resistance. Here we demonstrate that introduction of a tobacco phylloplanin gene—as a fusion with the GFP gene—targeted to the apoplasm can increase resistance to blue mold disease in a susceptible host tobacco. 相似文献9.
Edmond M. Linossi Indu R. Chandrashekaran Tatiana B. Kolesnik James M. Murphy Andrew I. Webb Tracy A. Willson Lukasz Kedzierski Alex N. Bullock Jeffrey J. Babon Raymond S. Norton Nicos A. Nicola Sandra E. Nicholson 《PloS one》2013,8(8)
Suppressor of Cytokine Signaling (SOCS)5 is thought to act as a tumour suppressor through negative regulation of JAK/STAT and epidermal growth factor (EGF) signaling. However, the mechanism/s by which SOCS5 acts on these two distinct pathways is unclear. We show for the first time that SOCS5 can interact directly with JAK via a unique, conserved region in its N-terminus, which we have termed the JAK interaction region (JIR). Co-expression of SOCS5 was able to specifically reduce JAK1 and JAK2 (but not JAK3 or TYK2) autophosphorylation and this function required both the conserved JIR and additional sequences within the long SOCS5 N-terminal region. We further demonstrate that SOCS5 can directly inhibit JAK1 kinase activity, although its mechanism of action appears distinct from that of SOCS1 and SOCS3. In addition, we identify phosphoTyr317 in Shc-1 as a high-affinity substrate for the SOCS5-SH2 domain and suggest that SOCS5 may negatively regulate EGF and growth factor-driven Shc-1 signaling by binding to this site. These findings suggest that different domains in SOCS5 contribute to two distinct mechanisms for regulation of cytokine and growth factor signaling. 相似文献
10.
Proline, a stress marker, is routinely quantified by a protocol that essentially uses hazardous toluene. Negative impacts of toluene on human health prompted us to develop a reliable alternate protocol for proline quantification. Absorbance of the proline-ninhydrin condensation product formed by reaction of proline with ninhydrin at 100 °C in the reaction mixture was significantly higher than that recorded after its transfer to toluene, revealing that toluene lowers sensitivity of this assay. λ max of the proline-ninhydrin complex in the reaction mixture and toluene were 508 and 513 nm, respectively. Ninhydrin in glacial acetic acid yielded higher quantity of the proline-ninhydrin condensation product compared to ninhydrin in mixture of glacial acetic acid and H3PO4, indicating negative impact of H3PO4 on proline quantification. Further, maximum yield of the proline-ninhydrin complex with ninhydrin in glacial acetic acid and ninhydrin in mixture of glacial acetic acid and H3PO4 was achieved within 30 and 60 min, respectively. This revealed that H3PO4 has negative impact on the reaction rate and quantity of the proline-ninhydrin complex formed. In brief, our proline quantification protocol involves reaction of a 1-ml proline sample with 2 ml of 1.25 % ninhydrin in glacial acetic acid at 100 °C for 30 min, followed by recording absorbance of the proline-ninhydrin condensation product in the reaction mixture itself at 508 nm. Amongst proline quantification protocols known till date, our protocol is the most simple, rapid, reliable, cost-effective, and eco-friendlier. 相似文献