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1.
Owing to the exceptional intracellular distribution and the heterogeneous expression pattern during transformation and metastasis
in various tumors, the EF-hand calcium-binding protein S100A2 attracts increasing attention. Unlike the majority of S100 proteins,
S100A2 expression is downregulated in many cancers and the loss in nuclear expression has been associated with poor prognosis.
On the other hand, S100A2 is upregulated in some cancers. This mini review highlights the general characteristics of S100A2
and discusses recent findings on its putative functional implication as a suppressor or promoter in cancerogenesis. 相似文献
2.
3.
Susann Eichenberger-Glinz 《Development genes and evolution》1979,186(4):333-349
Summary The present investigation analyzes intercellular junctions in tissues with different developmental capacities. The distribution of junctions was studied inDrosophila embryos, in imaginal disks, and in cultures of disk cells that were no longer able to differentiate any specific pattern of the adult epidermis.The first junctions —primitive desmosomes andclose membrane appositions — already appear in blastoderm.Gap junctions are first detected in early gastrulae and later become more and more frequent.Zonulae adhaerentes are formed around 6 h after fertilization, whileseptate junctions appear in the ectoderm of 10-h-old embryos.Inwing disks of all stages studied (22–120 h), three types of junctions are found: zonulae adhaereentes, gap junctions, and septate junctions. Gap junctions, which are rare and small at 22 h, increase in number and size during larval development. The other types of junctions are found between all cells of a wing disk throughout development.All types of junctions that are found in normal wing disks are also present in theimaginal disk tissues cultured in vivo for some 15 years and in thevesicles of imaginal disk cells grown in embryonic primary cultures in vitro. However, gap junctions are smaller and in the vesicles less frequent than in wing disks of mature larvae.Thus gap junctions, which allow small molecules to pass between the cells they connect, are present in the early embryo, when the first developmental decisions take place, and in all imaginal disk tissues studied, irrespective of whether or not these are capable of forming normal patterns. 相似文献
4.
5.
Susann Teneberg Timothy R. Hirst Jonas Ångström Karl-Anders Karlsson 《Glycoconjugate journal》1994,11(6):533-540
The binding specificities of cholera toxin andEscherichia coli heat-labile enterotoxin were investigated by binding of125I-labelled toxins to reference glycosphingolipids separated on thin-layer chromatograms and coated in microtitre wells. The binding of cholera toxin was restricted to the GM1 ganglioside. The heat-labile toxin showed the highest affinity for GM1 but also bound, though less strongly, to the GM2, GD2 and GD1b gangliosides and to the non-acid glycosphingolipids gangliotetraosylceramide and lactoneotetraosylceramide. The infant rabbit small intestine, a model system for diarrhoea induced by the toxins, was shown to contain two receptor-active glycosphingolipids for the heat-labile toxin, GM1 ganglioside and lactoneotetraosylceramide, whereas only the GM1 ganglioside was receptor-active for cholera toxin. Preliminary evidence was obtained, indicating that epithelial cells of human small intestine also contain lactoneotetraosylceramide and similar sequences. By computer-based molecular modelling, lactoneotetraosylceramide was docked into the active site of the heat-labile toxin, using the known crystal structure of the toxin in complex with lactose. Interactions which may explain the relatively high toxin affinity for this receptor were found.Abbreviations CT
cholera toxin
- CT-B
B-subunits of cholera toxin
- LT
Escherichia coli heat-labile enterotoxin
- hLT
humanEscherichia coli heat-labile enterotoxin
- pLT
porcineEscherichia coli heat-labile enterotoxin
- EI
electron ionization 相似文献
6.
T. Tvrdik Suzanne Marcus Sai-Mei Hou Susann Fält Peri Noori Natalia Podlutskaja Folker Hanefeld Petter Strømme Bo Lambert 《Human genetics》1998,103(3):311-318
Mutations identified in the hypoxanthine phosphoribosyltransferase (HPRT) gene of patients with Lesch-Nyhan (LN) syndrome
are dominated by simple base substitutions. Few hotspot positions have been identified, and only three large genomic rearrangements
have been characterized at the molecular level. We have identified one novel mutation, two tentative hot spot mutations, and
two deletions by direct sequencing of HPRT cDNA or genomic DNA from fibroblasts or T-lymphocytes from LN patients in five
unrelated families. One is a missense mutation caused by a 610C→T transition of the first base of HPRT exon 9. This mutation
has not been described previously in an LN patient. A nonsense mutation caused by a 508C→T transition at a CpG site in HPRT
exon 7 in the second patient and his younger brother is the fifth mutation of this kind among LN patients. Another tentative
hotspot mutation in the third patient, a frame shift caused by a G nucleotide insertion in a monotonous repeat of six Gs in
HPRT exon 3, has been reported previously in three other LN patients. The fourth patient had a tandem deletion: a 57-bp deletion
in an internally repeated Alu-sequence of intron 1 was separated by 14 bp from a 627-bp deletion that included HPRT exon 2 and was flanked by a 4-bp repeat.
This complex mutation is probably caused by a combination of homologous recombination and replication slippage. Another large
genomic deletion of 2969 bp in the fifth patient extended from one Alu-sequence in the promoter region to another Alu-sequence of intron 1, deleting the whole of HPRT exon 1. The breakpoints were located within two 39-bp homologous sequences,
one of which overlapped with a well-conserved 26-bp Alu-core sequence previously suggested as promoting recombination. These results contribute to the establishment of a molecular
spectrum of LN mutations, support previous data indicating possible mutational hotspots, and provide evidence for the involvement
of Alu-mediated recombination in HPRT deletion mutagenesis.
Received: 21 April 1998 / Accepted: 16 July 1998 相似文献
7.
The carbohydrate binding preferences of the Galalpha3Galbeta4 GlcNAc-binding lectins from Marasmius oreades and Euonymus europaeus were examined by binding to glycosphingolipids on thin-layer chromatograms and in microtiter wells. The M. oreades lectin bound to Galalpha3-terminated glycosphingolipids with a preference for type 2 chains. The B6 type 2 glycosphingolipid (Galalpha3[Fucalpha2]Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer) was preferred over the B5 glycosphingolipid (Galalpha3Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer), suggesting that the alpha2-linked Fuc is accommodated in the carbohydrate binding site, providing additional interactions. The lectin from E. europaeus had broader binding specificity. The B6 type 2 glycosphingolipid was the best ligand also for this lectin, but binding to the B6 type 1 glycosphingolipid (Galalpha3[Fucalpha2]Galbeta3GlcNAcbeta3Galbeta4Glcbeta1Cer) was also obtained. Furthermore, the H5 type 2 glycosphingolipid (Fucalpha2Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer), devoid of a terminal alpha3-linked Gal, was preferred over the the B5 glycosphingolipid, demonstrating a significant contribution to the binding affinity by the alpha2-linked Fuc. The more tolerant nature of the lectin from E. europaeus was also demonstrated by the binding of this lectin, but not the M. oreades lectin, to the x2 glycosphingolipid (GalNAcbeta3Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer) and GlcNAcbeta3Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer. The A6 type 2 glycosphingolipid (GalNAcalpha3[Fucalpha2]Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer) and GalNAcalpha3Galbeta4GlcNAcbeta3Galbeta4Glcbeta1-Cer were not recognized by the lectins despite the interaction with B6 type 2 glycosphingolipid and the B5 glycosphingolipid. These observations are explained by the absolute requirement of a free hydroxyl in the 2-position of Galalpha3 and that the E. europaea lectin can accommodate a GlcNAc acetamido moiety close to this position by reorienting the terminal sugar, whereas the M. oreades lectin cannot. 相似文献
8.
Thomas Jans Erika Graf Christian Jacob Ulrike Zwanzger Silke Groß-Lesch Swantje Matthies Evgeniy Perlov Klaus Hennighausen Melanie Jung Michael Rösler Monika Schulte-Altedorneburg Alexander von Gontard Susann Hänig Esther Sobanski Barbara Alm Luise Poustka Lucia Bliznak Michael Colla Laura Gentschow Roland Burghardt Harriet Salbach-Andrae Katja Becker Martin Holtmann Christine Freitag Andreas Warnke Alexandra Philipsen 《Attention deficit and hyperactivity disorders》2013,5(1):29-40
9.
Long X Lin Y Ortiz-Vega S Busch S Avruch J 《The Journal of biological chemistry》2007,282(25):18542-18551
The small GTPase Rheb is a positive upstream regulator of the target of rapamycin (TOR) complex 1 in mammalian cells and can bind directly to TOR complex 1. To identify the regions of the Rheb surface most critical for signaling to TOR complex 1, we created a set of 26 mutants wherein clusters of 1-5 putative solvent-exposed residues were changed to alanine, ultimately changing 65 residues distributed over the entire Rheb surface. The signaling function of these mutants was assessed by their ability, in comparison to wild type Rheb, to restore the phosphorylation of S6K1(Thr389) when expressed transiently in amino acid-deprived 293T cells. The major finding is that two mutants situated in the Rheb switch 2 segment, Y67A/I69A and I76A/D77A, exhibit a near total loss of function, whereas extensive replacement of the switch 1 segment and other surface residues with alanines causes relatively little disturbance of Rheb rescue of S6K1 from amino acid withdrawal. This is surprising in view of the minimal impact of guanyl nucleotide on Rheb switch 2 configuration. The loss of function Rheb switch 2 mutants are well expressed and exhibit partial agonist function in amino acid-replete cells. They are unimpaired in their ability to bind GTP or mammalian (m)TOR in vivo or in vitro, and the mTOR polypeptides retrieved with these inactive Rheb mutants exhibit kinase activity in vitro comparable with mTOR bound to wild type Rheb. We conclude that Rheb signaling to mTOR in vivo requires a Rheb switch 2-dependent interaction with an element other than the three known polypeptide components of TOR complex 1. 相似文献
10.
Hinney A Nguyen TT Scherag A Friedel S Brönner G Müller TD Grallert H Illig T Wichmann HE Rief W Schäfer H Hebebrand J 《PloS one》2007,2(12):e1361