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101.
The effects of coumarin on the translocation of 2,4,5-trichlorophenoxyaceticacid (2,4,5-T) in bean (Phaseolus vulgaris L. cv. StringlessGreenpod) seedlings was determined. 14C-labeled 2,4,5-T wasinjected in the stem tissue at the cotyledonary node along withthe coumarin or the coumarin was added to the nutrient solutionprior to, or at the time of, 2,4,5-T treatment. The amount oftranslocation of radioactive 2,4,5-T to plant parts was thendetermined at various times after treatment. An immediate effectof coumarin was to enhance acropetal 2,4,5-T translocation tothe young shoots. This effect occurred at low 2,4,5-T treatmentlevels and appeared to be specific for 2,4,5-T since sucrosetranslocation was not affected. Prolonged treatment with coumarininhibited acropetal and basipetal 2,4,5-T translocation in amanner similar to prolonged treatment with abscisic acid (ABA).Gibberellin A3 (GA) reversed the inhibitory effects of coumarinand ABA on 2,4,5-T acropetal translocation.
1 Journal article 3244 of the Agricultural Experiment Station,Oklahoma State University. (Received December 6, 1976; ) 相似文献
102.
Schuler P Assefa D Ylänne J Basler N Olschewski M Ahrens I Nordt T Bode C Peter K 《Cell communication & adhesion》2003,10(1):17-26
Implantation of stents into stenosed arteries helps to restore normal blood flow in ischemic organs. However, limited biocompatibility of the applied medical steel can cause acute thrombosis and long-term restenosis. Adhesion of monocytes to stent metal may participate in those acute and long-term complications of stent placement. Based on described prominent electrochemical properties of the interaction between the monocyte integrin receptor Mac-1 and its various ligands, we hypothesized, that this receptor is a central mediator of monocyte adhesion to stent metal and that semiconductor coating of medical steel reduces monocyte adhesion. Adhesion of monocytes on L-316 stainless steel was directly evaluated by light microscopy. Mac-1 could be identified as mediator of monocyte adhesion, since cell adhesion could be blocked by anti-Mac-1-antibodies, including the cross-reacting anti-GPIIb/IIIa antibody fragment abciximab. To further prove the central role of Mac-1, two CHO cell lines were generated expressing recombinant Mac-1 either as wild type, resulting in a low affinity receptor, or mutant with a GFFKR deletion of the alpha(M) subunit, resulting in a high affinity receptor. Indeed, adhesion was specific for Mac-1 and dependent on the affinity state of this integrin. Finally, we could demonstrate that Mac-1-mediated adhesion of monocytes to stents can be significantly inhibited by silicon carbide coating of the stent metal. In conclusion, the integrin Mac-1 and its affinity state could be identified as major mediators of monocyte adhesion on medical steel. As therapeutic strategies, the blockade of Mac-1 by antibodies or silicon carbide coating of steel inhibits monocyte adhesion on stents. 相似文献
103.
Immunoproteasomes down-regulate presentation of a subdominant T cell epitope from lymphocytic choriomeningitis virus 总被引:3,自引:0,他引:3
Basler M Youhnovski N Van Den Broek M Przybylski M Groettrup M 《Journal of immunology (Baltimore, Md. : 1950)》2004,173(6):3925-3934
The cytotoxic T cell response to pathogens is usually directed against a few immunodominant epitopes, while other potential epitopes are either subdominant or not used at all. In C57BL/6 mice, the acute cytotoxic T cell response against lymphocytic choriomeningitis virus is directed against immunodominant epitopes derived from the glycoprotein (gp33-41) and the nucleoprotein (NP396-404), while the gp276-286 epitope remains subdominant. Despite extensive investigations, the reason for this hierarchy between epitopes is not clear. In this study, we show that the treatment of cells with IFN-gamma enhanced the presentation of gp33-41, whereas presentation of the gp276-286 epitope from the same glycoprotein was markedly reduced. Because proteasomes are crucially involved in epitope generation and because IFN-gamma treatment in vitro and lymphocytic choriomeningitis virus infection in vivo lead to a gradual replacement of constitutive proteasomes by immunoproteasomes, we investigated the role of proteasome composition on epitope hierarchy. Overexpression of the active site subunits of immunoproteasomes LMP2, LMP7, and MECL-1 as well as overexpression of LMP2 alone suppressed the presentation of the gp276-286 epitope. The ability to generate gp276-286-specific CTLs was enhanced in LMP2- and LMP7-deficient mice, and macrophages from these mice showed an elevated presentation of this epitope. In vitro digests demonstrated that fragmentation by immunoproteasomes, but not constitutive proteasomes led to a preferential destruction of the gp276 epitope. Taken together, we show that LMP2 and LMP7 can at least in part determine subdominance and shape the epitope hierarchy of CTL responses in vivo. 相似文献
104.
Nipah virus V and W proteins have a common STAT1-binding domain yet inhibit STAT1 activation from the cytoplasmic and nuclear compartments, respectively 总被引:1,自引:0,他引:1 下载免费PDF全文
In previous reports it was demonstrated that the Nipah virus V and W proteins have interferon (IFN) antagonist activity due to their ability to block signaling from the IFN-alpha/beta receptor (J. J. Rodriguez, J. P. Parisien, and C. M. Horvath, J. Virol. 76:11476-11483, 2002; M. S. Park et al., J. Virol. 77:1501-1511, 2003). The V, W, and P proteins are all encoded by the same viral gene and share an identical 407-amino-acid N-terminal region but have distinct C-terminal sequences. We now show that the P protein also has anti-IFN function, confirming that the common N-terminal domain is responsible for the antagonist activity. Truncation of this N-terminal domain revealed that amino acids 50 to 150 retain the ability to block IFN and to bind STAT1, a key component of the IFN signaling pathway. Subcellular localization studies demonstrate that the V and P proteins are predominantly cytoplasmic whereas the W protein is localized to the nucleus. In all cases, STAT1 colocalizes with the corresponding Nipah virus protein. These interactions are sufficient to inhibit STAT1 activation, as demonstrated by the lack of STAT1 phosphorylation on tyrosine 701 in IFN-stimulated cells expressing P, V, or W. Therefore, despite their common STAT1-binding domain, the Nipah virus V and P proteins act by retaining STAT1 in the cytoplasm while the W protein sequesters STAT1 in the nucleus, creating both a cytoplasmic and a nuclear block for STAT1. We also show that the IFN antagonist activity of the P protein is not as strong as that of V or W, perhaps explaining why Nipah virus has evolved to express these two edited products. 相似文献
105.
dMyc transforms cells into super-competitors 总被引:8,自引:0,他引:8
Overexpression of myc protooncogenes has been implicated in the genesis of many human tumors. Myc proteins seem to regulate diverse biological processes, but their role in tumorigenesis remains enigmatic. Here we use Drosophila imaginal discs to mimic situations in which cells with unequal levels of Myc protein are apposed and show that this invariably elicits a win/lose situation reminiscent of cell competition; cells with lower levels of dMyc are eliminated by apoptosis whereas cells with higher levels of dMyc over-proliferate. We find that this competitive behavior correlates with, and can be corrected by, the activation of the BMP/Dpp survival signaling pathway. Hence the heritable increase in dMyc levels causes cells to behave as "super-competitors" and reveals a novel mode of clonal expansion that causes, but also relies on, the killing of surrounding cells. 相似文献
106.
Polymorphism and divergence at the 5' flanking region of the sex- determining locus, Sry, in mice 总被引:3,自引:0,他引:3
We have investigated patterns of evolution in the nonrecombining portion of
the Y chromosome in mice by comparing levels of polymorphism within Mus
domesticus with levels of divergence between M. domesticus and M. spretus.
A 1,277-bp fragment of noncoding sequence flanking the sex determining
locus (Sry) was PCR amplified, and 1,063 bases were sequenced and compared
among 20 M. domesticus and 1 M. spretus. Two polymorphic base substitutions
and two polymorphic insertion/deletion sites were identified within M.
domesticus; nucleotide diversity was estimated to be 0.1%. Divergence
between M. domesticus and M. spretus for this region (1.9%) was slightly
lower than the average divergence of single-copy nuclear DNA for these
species. Comparison of levels of polymorphism and divergence at Sry with
levels of polymorphism and divergence in the mitochondrial DNA control
region provided no evidence of a departure from the expectations of neutral
molecular evolution. These findings are consistent with the presumed lack
of function for much of the Y chromosome.
相似文献
107.
Zhaoming Su Chao Wu Liuqing Shi Priya Luthra Grigore D. Pintilie Britney Johnson Justin R. Porter Peng Ge Muyuan Chen Gai Liu Thomas E. Frederick Jennifer M. Binning Gregory R. Bowman Z. Hong Zhou Christopher F. Basler Michael L. Gross Daisy W. Leung Wah Chiu Gaya K. Amarasinghe 《Cell》2018,172(5):966-978.e12
108.
K Basler B Oesch M Scott D Westaway M W?lchli D F Groth M P McKinley S B Prusiner C Weissmann 《Cell》1986,46(3):417-428
109.
The genotoxicity of 51 epoxides is studied with the SOS-Chromotest using Escherichia coli PQ37 as tester strain. The results obtained with this test system are compared with results of the Ames test. Out of 51 epoxides, 39 are shown to be mutagenic in Salmonella typhimurium whereas only 27 mutagenic epoxides induced the SOS response in Escherichia coli PQ37. 相似文献
110.
Osvaldo Martinez Joshua Johnson Balaji Manicassamy Lijun Rong Gene G. Olinger Lisa E. Hensley Christopher F. Basler 《Cellular microbiology》2010,12(2):148-157
Cathepsins B and L contribute to Ebola virus (EBOV) entry into Vero cells and mouse embryonic fibroblasts. However, the role of cathepsins in EBOV‐infection of human dendritic cells (DCs), important targets of infection in vivo, remains undefined. Here, EBOV‐like particles containing a β‐lactamase–VP40 fusion reporter and Ebola virus were used to demonstrate the cathepsin dependence of EBOV entry into human monocyte‐derived DCs. However, while DC infection is blocked by cathepsin B inhibitor, it is insensitive to cathepsin L inhibitor. Furthermore, DCs pre‐treated for 48 h with TNFα were generally less susceptible to entry and infection by EBOV. This decrease in infection was associated with a decrease in cathepsin B activity. Thus, cathepsin L plays a minimal, if any, role in EBOV infection in human DCs. The inflammatory cytokine TNFα modulates cathepsin B activity and affects EBOV entry into and infection of human DCs. 相似文献