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101.
Sengupta R Sahoo R Ray SS Dutta T Dasgupta A Ghosh S 《Molecular and cellular biochemistry》2006,284(1-2):117-126
The oxygenase domain of the inducible nitric oxide synthase, Δ65 iNOSox is a dimer that binds heme, L-Arginine (L-Arg), and tetrahydrobiopterin (H4B) and is the site for NO synthesis. The role of H4B in iNOS structure-function is complex and its exact structural role is presently unknown. The present paper provides a simple
mechanistic account of interaction of the cofactor tetrahydrobiopterin (H4B) with the bacterially expressed Δ65 iNOSox protein. Transverse urea gradient gel electrophoresis studies indicated the presence
of different conformers in the cofactor-incubated and cofactor-free Δ65 iNOSox protein. Dynamic Light Scattering (DLS) studies
of cofactor-incubated and cofactor-free Δ65 iNOSox protein also showed two distinct populations of two different diameter
ranges. Cofactor tetrahydrobiopterin (H4B) shifted one population, with higher diameter, to the lower diameter ranges indicating conformational changes. The additional
role played by the cofactor is to elevate the heme retaining capacity even in presence of denaturing stress. Together, these
findings confirm that the H4B is essential in modulating the iNOS heme environment and the protein environment in the dimeric iNOS oxygenase domain. (Mol
Cell Boichem xxx: 1–10, 2005)
Supported by Calcutta University Research Grants. 相似文献
102.
Arghya Basu Soma Bhattacharyya Paramita Chaudhuri Subhabrata Sengupta Anil K. Ghosh 《Biochimica et Biophysica Acta (BBA)/General Subjects》2006
Two haploid strains of Saccharomyces cerevisiae viz. MATα and MATa were grown in glucose and trehalose medium and growth patterns were compared. Both strains show similar growth, except for an extended lag phase in trehalose grown cells. In both trehalose grown strains increase in activities of both extracellular trehalase activities and simultaneous decrease in extracellular trehalose level was seen. This coincided with a sharp increase in extracellular glucose level and beginning of log phase of growth. Alcohol production was also observed. Secreted trehalase activity was detected, in addition to periplasmic activity. It appeared that extracellular trehalose was hydrolyzed into glucose by extracellular trehalase activity. This glucose was utilized by the cells for growth. The alcohol formation was due to the fermentation of glucose. Addition of extracellular trehalase caused reduction in the lag phase when grown in trehalose medium, supporting our hypothesis of extracellular utilization of trehalose. 相似文献
103.
104.
Chaudhuri RK Mukherjee M Sengupta D Mazumder S 《Indian journal of experimental biology》2006,44(3):254-255
The most widely used method for estimation of plasma glucose is that adopted by Trinder's using glucose oxidase-peroxidase (GOD-POD) system. This method gives much lower blood glucose values with blood samples of neonatal jaundice (plasma bilirubin level > 10 mg/dL) of age 10 +/- 5 daysthan with samples of neonates of the same age group without jaundice or older children suffering from other diseases like acute respiratory distress, septicemia. 相似文献
105.
Members of the HES subfamily of bHLH proteins play crucial roles in neural patterning via repression of neurogenesis. In C. elegans, loss-of-function mutations in ref-1, a distant nematode-specific member of this subfamily, were previously shown to cause ectopic neurogenesis from postembryonic lineages. However, while the vast majority of the nervous system in C. elegans is generated embryonically, the role of REF-1 in regulating these neural lineage decisions is unknown. Here, we show that mutations in ref-1 result in the generation of multiple ectopic neuron types derived from an embryonic neuroblast. In wild-type animals, neurons derived from this sublineage are present in a left/right symmetrical manner. However, in ref-1 mutants, while the ectopically generated neurons exhibit gene expression profiles characteristic of neurons on the left, they are present only on the right side. REF-1 functions in a Notch-independent manner to regulate this ectopic lineage decision. We also demonstrate that loss of REF-1 function results in defective differentiation of an embryonically generated serotonergic neuron type. These results indicate that REF-1 functions in both Notch-dependent and independent pathways to regulate multiple developmental decisions in different neuronal sublineages. 相似文献
106.
Garai K Sengupta P Sahoo B Maiti S 《Biochemical and biophysical research communications》2006,345(1):210-215
Aggregation of the amyloid beta (Abeta) peptide yields both fibrillar precipitates and soluble oligomers, and is associated with Alzheimer's disease (AD). In vitro, Cu(2+) and Zn(2+) strongly bind Abeta and promote its precipitation. However, less is known about their interactions with the soluble oligomers, which are thought to be the major toxic species responsible for AD. Using fluorescence correlation spectroscopy to resolve the various soluble species of Abeta, we show that low concentrations of Cu(2+) (1 microM) and Zn(2+) (4 microM) selectively eliminate the oligomeric population (within approximately 2h), while Mg(2+) displays a similar effect at a higher concentration (60 microM). This uncovers a new aspect of Abeta-metal ion interactions, as precipitation is not substantially altered at these low metal ion concentrations. Our results suggest that physiological concentrations of Cu(2+) and Zn(2+) can critically alter the stability of the toxic Abeta oligomers and can potentially control the course of neurodegeneration. 相似文献
107.
Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB 总被引:15,自引:0,他引:15
Sarbassov DD Ali SM Sengupta S Sheen JH Hsu PP Bagley AF Markhard AL Sabatini DM 《Molecular cell》2006,22(2):159-168
The drug rapamycin has important uses in oncology, cardiology, and transplantation medicine, but its clinically relevant molecular effects are not understood. When bound to FKBP12, rapamycin interacts with and inhibits the kinase activity of a multiprotein complex composed of mTOR, mLST8, and raptor (mTORC1). The distinct complex of mTOR, mLST8, and rictor (mTORC2) does not interact with FKBP12-rapamycin and is not thought to be rapamycin sensitive. mTORC2 phosphorylates and activates Akt/PKB, a key regulator of cell survival. Here we show that rapamycin inhibits the assembly of mTORC2 and that, in many cell types, prolonged rapamycin treatment reduces the levels of mTORC2 below those needed to maintain Akt/PKB signaling. The proapoptotic and antitumor effects of rapamycin are suppressed in cells expressing an Akt/PKB mutant that is rapamycin resistant. Our work describes an unforeseen mechanism of action for rapamycin that suggests it can be used to inhibit Akt/PKB in certain cell types. 相似文献
108.
109.
110.
Siddhartha S. Saha Pritha Dasgupta Sumita Sengupta Mahua Ghosh 《Biochimica et Biophysica Acta (BBA)/General Subjects》2012