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41.
Neuronal differentiation-dependent expression of the disialic acid epitope on CD166 and its involvement in neurite formation in Neuro2A cells 总被引:4,自引:0,他引:4
We previously demonstrated that alpha2,8-linked disialic acid (diSia) residues occur in several glycoproteins of mammalian brains (Sato, C., Fukuoka, H., Ohta, K., Matsuda, T., Koshino, R., Kobayashi, K., Troy, F. A., II, and Kitajima, K. (2000) J. Biol. Chem. 275, 15422-15431). The role of the diSia epitope on these glycoproteins is not known, whereas the importance of the diSia epitope on glycolipids is well documented in neurite formation. In this study, we demonstrated that the diSia epitope (Neu5Acalpha2 --> 8Neu5Acalpha2 --> 3Gal) on glycoproteins, but not on glycolipids, is involved in neurite formation in a mouse neuroblastoma cell line, Neuro2A, based on the following lines of evidence. First, the amount of diSia epitope on glycoproteins increased during retinoic acid-induced neurite formation. Second, retinoic acid treatment primarily increased the diSia epitope on a 100-kDa glycoprotein. We identified this protein as CD166 (SC1), an immunoglobulin superfamily cell adhesion molecule involved in neurite extension. Third, a monoclonal antibody against the diSia epitope specifically inhibited neurite formation. We also demonstrated that alpha2,8-sialyltransferase III mRNA expression increased 1.7-fold after the induction of neurite formation, suggesting that alpha2,8-sialyltransferase III is responsible for formation of the diSia epitope on CD166. 相似文献
42.
Prostaglandin (PG) F(2alpha), one of the primary prostanoids generated in vascular tissue, is known to cause hypertrophy in vascular smooth muscle cells. To clarify the molecular mechanisms underlying PGF(2alpha)-induced hypertrophy, the involvement of reactive oxygen species was examined in a rat vascular smooth muscle cell line, A7r5. PGF(2alpha) and (+)-fluprostenol, a selective agonist of the PGF receptor, significantly increased intracellular O(2)(-) in A7r5. The PGF(2alpha)-induced O(2)(-) increase was suppressed by diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase that has been reported to be the major source of O(2)(-) in vascular cells. The augmented synthesis of the protein induced by PGF(2alpha) or (+)-fluprostenol was suppressed in the presence of DPI. In PGF(2alpha) or (+)-fluprostenol-treated cells, a dose-dependent increase in the expression of NOX1, a homolog of the catalytic subunit of the phagocyte NADPH oxidase gp91(phox), was demonstrated by Northern blot analysis. Finally, depletion of NOX1 mRNA in the cells transfected with ribozymes targeted for three independent cleavage sites on the mRNA sequence significantly reduced the PGF(2alpha)-induced increase in protein synthesis. Taken together, these results suggest that hypertrophy of vascular smooth muscle cells caused by PGF(2alpha) is mediated by NOX1 induction and the resultant overproduction of O(2)(-) by NADPH oxidase. 相似文献
43.
Chihiro Kachi-TerajimaHitoshi Miyasaka Tomohiko IshiiKen-ichi Sugiura Masahiro Yamashita 《Inorganica chimica acta》2002,332(1):210-215
The ligand substitution reaction of Ru2(O2CCH3)4Cl with 2-amino-4,6-dimethylpyrimidine (Hadmpym) under gentle refluxing conditions in methanol led to the formation of a bridging-ligand mono-substituted compound, [Ru2(O2CCH3)3(admpym)(Cl)(MeOH)] (1). Compound 1 crystallized in monoclinic space group P21/n (no. 14) with a=8.3074(8) Å, b=12.3722(8) Å, c=18.913(1) Å, β=95.559(3)°, V=1934.8(3) Å3, and Z=4. Temperature dependence of the magnetic susceptibility of 1 revealed it to be in a spin ground state S=3/2 arising from the electronic configuration of σ2π4δ2(δ*π*)3. Compound 1 undergoes three metal-centered redox reactions in electrochemistry: E1/2 (ox)=+0.72 V (Ia/Ic<1, ΔEp=0.17 V); E1/2 (1,red)=−0.65 V (Ia/Ic≈1, ΔEp=0.10 V); and E1/2 (2,red)=−1.80 V (Ia/Ic?1, ΔEp=0.16 V). Then, the redox species produced by electrolysis were characterized by spectroscopic studies. 相似文献
44.
Ogawa T Ishii C Suda Y Kamiya H Muramoto K 《Bioscience, biotechnology, and biochemistry》2002,66(2):476-480
An expression system for recombinant conger eel galectins, congerins I and II, were constructed using the pTV 118N plasmid vector and Escherichia coli. Recombinant congerins I and II could be obtained in the soluble active form with high quantitative yield. Mutation of codons for Val and Leu located in the N-terminal region of Con I increased the expression efficiency. Purification of recombinant proteins were done by only two chromatographical steps from E. coli extract. The purified recombinant congerins were found to be almost the same as the native ones except for the acetyl group at the N-terminus; that is, they showed the same structures and carbohydrate binding activities, suggesting that N-terminal acetyl groups of congerins were not significant for activity. 相似文献
45.
46.
Aciculosporium take (Ascomycota; Clavicipitaceae), causes the witches' broom disease in bamboo, particularly Phyllostachys bambusoides. Since it was observed that endogenous indole-3-acetic acid is reduced in the twigs of the diseased bamboo, the symptoms (bushy appearance) may be induced by reduction in auxin levels. Furthermore, two indolic compounds accumulated in diseased twigs, these being identified as N-p-coumaroylserotonin and N-feruloylserotonin by LC-MS, 1H NMR and 13C NMR spectroscopic analyses. N-p-Coumaroylserotonin possesses antifungal activity against A. take. 相似文献
47.
Shigella deliver a subset of effector proteins such as IpaA, IpaB and IpaC via the type III secretion system (TTSS) into host cells during the infection of colonic epithelial cells. Many bacterial effectors including some from Shigella require specific chaperones for protection from degradation and targeting to the TTSS. In this study, we have investigated the role of the icsB gene located upstream of the ipaBCDA operon in Shigella infection because the role of IcsB as a virulence factor remains unknown. Here, we found that the IcsB protein is secreted via the TTSS of Shigella in vitro and in vivo. We show that IpgA protein encoded by ipgA, the gene immediately downstream of icsB, serves as the chaperone required for the stabilization and secretion of IcsB. We have shown that IcsB binds to IpgA in bacterial cytosol and the binding site is in the middle of the IcsB protein. Intriguingly, although its significance in Shigella pathogenicity is as yet unclear, the icsB gene can be read-through into the ipgA gene to create a translational fusion protein. Furthermore, the contribution of IcsB to the pathogenicity of Shigella was demonstrated by plaque-forming assay and the Sereny test. The ability of the icsB mutant to form plaques was greatly reduced compared with that of the wild type in MDCK cell monolayers. Furthermore, when guinea pig eyes were infected with a non-polar icsB mutant, the bacteria failed to provoke keratoconjunctivitis. These results suggest that IcsB is secreted via the TTSS, chaperoned by IpgA, and required at the post-invasion stage of Shigella pathogenicity 相似文献
48.
Kaoru Ohta Chihiro Sato Tsukasa Matsuda Masaru Toriyama Victor D. Vacquier William J. Lennarz Ken Kitajima 《Glycoconjugate journal》2000,17(3-4):205-214
The low density, detergent-insoluble membrane fraction (LD-DIM), where gangliosides are likely to be highly enriched, was prepared from sperm of two sea urchin species, Hemicentrotus pulcherrimus and Strongylocentrotus purpuratus. Immunoblotting showed the presence in the LD-DIM of two receptors for egg ligands, a glycosylphosphatidylinositol (GPI)-anchored protein, and four proteins which may be involved in signal transduction. Co-immunoprecipitation revealed that at least three proteins, the speract receptor, the 63[emsp4 ]kDa GPI-anchored protein and the subunit of a heterotrimeric Gs protein, are localized in the LD-DIM. This suggests that the LD-DIM fraction may be a membrane microdomain for speract–speract receptor interaction, as well as the subsequent signal transduction pathway involved in induction of sperm respiration, motility and possibly the acrosome reaction. 相似文献
49.
Abdul Gafur Chihiro Tanaka Kiminori Shimizu Seiji Ouchi Mitsuya Tsuda 《Mycoscience》1998,39(2):155-159
Nine polyoxin-resistant mutants ofCochliobolus heterostrophus were isolated after ethyl methanesulphonate mutagenesis. All were highly resistant to polyoxin (MIC≥1,600 ppm). Crosses between
the mutants and a wild-type strain revealed that the resistance trait was inherited to the offsprings in different fashions.
Four of the mutant strains inherited polyoxin resistance in a 1∶1 segregation ratio, indicating that the phenotypes in these
strains were due to alteration at a single locus. Allelism tests revealed four new loci,Pol1, Pol2, Pol3 andPol4, for polyoxin resistance in these mutant strains. The genes responsible for the phenotypes of the other five mutant strains
were not determined, because of extremely slow growth of progenies in one cross, sterility in another cross, and inexplicable
responses to polyoxin of the progenies in the other crosses. No linkage was detected between the genes for polyoxin resistance
and mating type. 相似文献
50.
Nobutake Yamamichi Takeshi Shimamoto Yu Takahashi Yoshiki Sakaguchi Hikaru Kakimoto Rie Matsuda Yosuke Kataoka Itaru Saito Yosuke Tsuji Seiichi Yakabi Chihiro Takeuchi Chihiro Minatsuki Keiko Niimi Itsuko Asada-Hirayama Chiemi Nakayama Satoshi Ono Shinya Kodashima Daisuke Yamaguchi Mitsuhiro Fujishiro Yutaka Yamaji Ryoichi Wada Toru Mitsushima Kazuhiko Koike 《PloS one》2015,10(4)