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R Selvatici M Rubini P Orlando A Balboni S Balugani E Gandini 《Biochemistry international》1991,25(1):151-158
HLA class I antigens seem to be involved in the proliferative response of PHA-activated human T-lymphocytes. We have previously reported that the treatment of PHA-activated peripheral blood mononuclear cells (PBMC) with an anti-HLA class I monoclonal antibody, 01.65, (i) inhibits the tritiated thymidine incorporation, (ii) inactivates cytosolic protein kinase C (PKC) and (iii) causes an increase in the duration of the cell cycle. Northern Blot kinetic analysis of c-fos, c-myc, cdc2, IL-2R, c-myb, ODC, TK and H3, from 10 minutes to 120 hours, was performed in MAb 01.65 treated cultures. We found that the expression of four genes (c-myc, IL-2R, cdc2 and TK) was depressed 24 hours after PHA stimulation. 相似文献
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Structural basis for the recruitment of ERCC1-XPF to nucleotide excision repair complexes by XPA
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Tsodikov OV Ivanov D Orelli B Staresincic L Shoshani I Oberman R Schärer OD Wagner G Ellenberger T 《The EMBO journal》2007,26(22):4768-4776
The nucleotide excision repair (NER) pathway corrects DNA damage caused by sunlight, environmental mutagens and certain antitumor agents. This multistep DNA repair reaction operates by the sequential assembly of protein factors at sites of DNA damage. The efficient recognition of DNA damage and its repair are orchestrated by specific protein-protein and protein-DNA interactions within NER complexes. We have investigated an essential protein-protein interaction of the NER pathway, the binding of the XPA protein to the ERCC1 subunit of the repair endonuclease ERCC1-XPF. The structure of ERCC1 in complex with an XPA peptide shows that only a small region of XPA interacts with ERCC1 to form a stable complex exhibiting submicromolar binding affinity. However, this XPA peptide is a potent inhibitor of NER activity in a cell-free assay, blocking the excision of a cisplatin adduct from DNA. The structure of the peptide inhibitor bound to its target site reveals a binding interface that is amenable to the development of small molecule peptidomimetics that could be used to modulate NER repair activities in vivo. 相似文献
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Marcelo De Franco Patrícia dos Santos Carneiro Luciana Carla Peters Francisca Vorraro Andrea Borrego Orlando Garcia Ribeiro Nancy Starobinas Wafa Koury Cabrera Olga Martinez Ibañez 《Mammalian genome》2007,18(4):263-269
Lines of mice were obtained by selective breeding for maximum (AIRmax) or minimum (AIRmin) acute inflammation. They present
distinct neutrophil influx and show frequency disequilibrium of the solute carrier family 11a member 1
(Slc11a1) alleles. This gene is involved in ion transport at the endosomes within macrophages and neutrophils, interfering in their
activation. Homozygous AIRmax and AIRmin sublines for the Slc11a1 gene were produced to examine the interaction of this gene with the acute inflammatory loci. The present work investigated
wound-healing traits in AIRmax and AIRmin mice, in F1 and F2 intercrosses, and in Slc11a1 sublines. Two-millimeter ear punches were made in the mice and hole closure was measured during 40 days. AIRmax mice demonstrated
significant tissue repair while AIRmin mice did not. Significant differences between the responses of male and female mice
were also observed. Wound-healing traits demonstrated a correlation with neutrophil influx in F2 populations. AIRmax
SS
showed higher ear-wound closure than AIRmax
RR
mice, suggesting that the Slc11a1
S allele favored ear tissue repair. QTL analysis has detected two inflammatory loci modulating ear wound healing on chromosomes
1 and 14. These results suggest the involvement of the acute inflammation modifier QTL in the wound-healing phenotype. 相似文献
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Levasseur A Orlando L Bailly X Milinkovitch MC Danchin EG Pontarotti P 《Biological reviews of the Cambridge Philosophical Society》2007,82(4):551-572
To demonstrate that a given change in the environment has contributed to the emergence of a given genotypic and phenotypic shift during the course of evolution, one should ask to what extent such shifts would have occurred without environmental change. Of course, such tests are rarely practical but phenotypic novelties can still be correlated to genomic shifts in response to environmental changes if enough information is available. We surveyed and re-evaluated the published data in order to estimate the role of environmental changes on the course of species and genomic evolution. Only a few published examples clearly demonstrate a causal link between a given environmental change and the fixation of a genomic variant resulting in functional modification (gain, loss or alteration of function). Many others suggested a link between a given phenotypic shift and a given environmental change but failed to identify the underlying genomic determinant(s) and/or the associated functional consequence(s). The proportion of genotypic and phenotypic variation that is fixed concomitantly with environmental changes is often considered adaptive and hence, the result of positive selection, even though alternative causes, such as genetic drift, are rarely investigated. Therefore, the second aim herein is to review evidence for the mechanisms leading to fixation. 相似文献