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41.
Interaction of leucerne saponins with steroids 总被引:2,自引:0,他引:2
B Gestetner Y Assa Y Henis Y Tencer M Rotman Y Birk A Bondi 《Biochimica et biophysica acta》1972,270(1):181-187
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Nan-Nan Niu Lu Lu Pan-Pan Peng Zhi-Juan Fu Dan Miao Ming Zhou Dror Noy Kai-Hong Zhao 《The Plant journal : for cell and molecular biology》2021,107(5):1420-1431
The phycobilisomes (PBSs) of cyanobacteria and red-algae are unique megadaltons light-harvesting protein-pigment complexes that utilize bilin derivatives for light absorption and energy transfer. Recently, the high-resolution molecular structures of red-algal PBSs revealed how the multi-domain core-membrane linker (LCM) specifically organizes the allophycocyanin subunits in the PBS’s core. But, the topology of LCM in these structures was different than that suggested for cyanobacterial PBSs based on lower-resolution structures. Particularly, the model for cyanobacteria assumed that the Arm2 domain of LCM connects the two basal allophycocyanin cylinders, whereas the red-algal PBS structures revealed that Arm2 is partly buried in the core of one basal cylinder and connects it to the top cylinder. Here, we show by biochemical analysis of mutations in the apcE gene that encodes LCM, that the cyanobacterial and red-algal LCM topologies are actually the same. We found that removing the top cylinder linker domain in LCM splits the PBS core longitudinally into two separate basal cylinders. Deleting either all or part of the helix-loop-helix domain at the N-terminal end of Arm2, disassembled the basal cylinders and resulted in degradation of the part containing the terminal emitter, ApcD. Deleting the following 30 amino-acids loop severely affected the assembly of the basal cylinders, but further deletion of the amino-acids at the C-terminal half of Arm2 had only minor effects on this assembly. Altogether, the biochemical data are consistent with the red-algal LCM topology, suggesting that the PBS cores in cyanobacteria and red-algae assemble in the same way. 相似文献
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Farnaz Assa Hossein Ajamein Hamideh Vaghari Omid Ahmadi 《Critical reviews in biotechnology》2017,37(4):492-509
The potential of magnetic nanoparticles (MNPs) in drug delivery systems (DDSs) is mainly related to its magnetic core and surface coating. These coatings can eliminate or minimize their aggregation under physiological conditions. Also, they can provide functional groups for bioconjugation to anticancer drugs and/or targeted ligands. Chitosan, as a derivative of chitin, is an attractive natural biopolymer from renewable resources with the presence of reactive amino and hydroxyl functional groups in its structure. Chitosan nanoparticles (NPs), due to their huge surface to volume ratio as compared to the chitosan in its bulk form, have outstanding physico-chemical, antimicrobial and biological properties. These unique properties make chitosan NPs a promising biopolymer for the application of DDSs. In this review, the current state and challenges for the application magnetic chitosan NPs in drug delivery systems were investigated. The present review also revisits the limitations and commercial impediments to provide insight for future works. 相似文献
45.
Clearance of dying cells and systemic lupus erythematosus: the role of C1q and the complement system
Dror Mevorach 《Apoptosis : an international journal on programmed cell death》2010,15(9):1114-1123
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease of unknown etiology characterized by the presence of
pathogenic high-titer autoantibodies to a diverse group of autoantigens. In 88% of patients, autoantibodies are present an
average of 3.3 years before diagnosis. Antinuclear, anti-Ro, anti-La, and anti-phospholipid antibodies appear first, followed
by anti-DNA, anti-Smith and anti-ribonucleoprotein. These autoantibodies have features of an antigen-driven, T-cell-dependent
immune response. Once present, the course of SLE is characterized by disease flares and autoimmune dysregulation. Programmed
cell death (PCD), an essential developmental and homeostatic mechanism, is the preferred physiological death processes for
cells as well as an important immune response regulator. Appropriate clearance of apoptotic material completes the PCD process,
and is essential for regulating of inflammation and maintaining self-tolerance. Early complement proteins are important in
protecting humans against the development of SLE and the protective role of C1q and complement in SLE is mainly related to
their role in clearance of dying cells. However, the complement system is also an important ingredient in inflammation, which
mediates SLE pathogenesis. Thus, the question remains whether complement factors have either a protective or a destructive
role, or a combination of both. 相似文献
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In vivo identification of tumor- suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma 总被引:6,自引:0,他引:6
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Gaussian network model (GNM) modes of motion are calculated to a dataset of h emoglobin (Hb) structures and modes with dynamics similarity to the T state are multiply aligned. The sole criterion for the alignment is the mode shape itself and not sequence or structural similarity. Standard deviation (SD) of the GNM value score along the alignment is calculated, regions with high SD are defined as dynamically variable. The analysis shows that the α1β1/α2β2 interface is a dynamically variable region but not the α1β2/α2β1 and the α1α2/β1β2 interfaces. The results are in accordance with the T → R2 transition of Hb. We suggest that dynamically variable regions are regions that are likely to undergo structural change in the protein upon binding, conformational transition, or any other relevant chemical event. The represented technique of multiple dynamics ‐ based alignment of modes is novel and may offer a new insight in proteins ' dynamics to function relation. Proteins 2014; 82:2097–2105. © 2014 Wiley Periodicals, Inc. 相似文献
50.
Amiel A. Dror Danielle R. Lenz Shaked Shivatzki Keren Cohen Osnat Ashur-Fabian Karen B. Avraham 《Mammalian genome》2014,25(7-8):304-316
Thyroid hormone is essential for inner ear development and is required for auditory system maturation. Human mutations in SLC26A4 lead to a syndromic form of deafness with enlargement of the thyroid gland (Pendred syndrome) and non-syndromic deafness (DFNB4). We describe mice with an Slc26a4 mutation, Slc26a4 loop/loop , which are profoundly deaf but show a normal sized thyroid gland, mimicking non-syndromic clinical signs. Histological analysis of the thyroid gland revealed defective morphology, with a majority of atrophic microfollicles, while measurable thyroid hormone in blood serum was within the normal range. Characterization of the inner ear showed a spectrum of morphological and molecular defects consistent with inner ear pathology, as seen in hypothyroidism or disrupted thyroid hormone action. The pathological inner ear hallmarks included thicker tectorial membrane with reduced β-tectorin protein expression, the absence of BK channel expression of inner hair cells, and reduced inner ear bone calcification. Our study demonstrates that deafness in Slc26a4 loop/loop mice correlates with thyroid pathology, postulating that sub-clinical thyroid morphological defects may be present in some DFNB4 individuals with a normal sized thyroid gland. We propose that insufficient availability of thyroid hormone during inner ear development plays an important role in the mechanism underlying deafness as a result of SLC26A4 mutations. 相似文献