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M. Frank I. Albrecht W. W. Sleator R. B. Robinson 《Cellular and molecular life sciences : CMLS》1975,31(5):578-580
Zusammenfassung Mit morphometrischen Methoden wurde beim Meerschweinchen eine quantitative Analyse von Volumen und Oberflächenareal der Ultrastrukturkomponenten der Herzvorhof-Muskulatur durchgeführt, die mit dem Erregungs-Kontraktions-Kopplungsvorgang und der Erschlaffung verknüpft sind. 相似文献
166.
P. de Mayo J. R. Robinson E. Y. Spencer R. W. White 《Cellular and molecular life sciences : CMLS》1962,18(8):359-360
Zusammenfassung Die Biogenese des Pilzstoffes Helminthosporal wurde untersucht, indem der Pilz bei Anwesenheit von Mevalonsäure, mit C2 mit Kohlenstoff-14 markiert, gezüchtet wurde. Es wird gezeigt, dass das Dialdehyd aus einem tricyclischen Vorläufer durch oxidative Spaltung entsteht. 相似文献
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Carpten JD Robbins CM Villablanca A Forsberg L Presciuttini S Bailey-Wilson J Simonds WF Gillanders EM Kennedy AM Chen JD Agarwal SK Sood R Jones MP Moses TY Haven C Petillo D Leotlela PD Harding B Cameron D Pannett AA Höög A Heath H James-Newton LA Robinson B Zarbo RJ Cavaco BM Wassif W Perrier ND Rosen IB Kristoffersson U Turnpenny PD Farnebo LO Besser GM Jackson CE Morreau H Trent JM Thakker RV Marx SJ Teh BT Larsson C Hobbs MR 《Nature genetics》2002,32(4):676-680
We report here the identification of a gene associated with the hyperparathyroidism-jaw tumor (HPT-JT) syndrome. A single locus associated with HPT-JT (HRPT2) was previously mapped to chromosomal region 1q25-q32. We refined this region to a critical interval of 12 cM by genotyping in 26 affected kindreds. Using a positional candidate approach, we identified thirteen different heterozygous, germline, inactivating mutations in a single gene in fourteen families with HPT-JT. The proposed role of HRPT2 as a tumor suppressor was supported by mutation screening in 48 parathyroid adenomas with cystic features, which identified three somatic inactivating mutations, all located in exon 1. None of these mutations were detected in normal controls, and all were predicted to cause deficient or impaired protein function. HRPT2 is a ubiquitously expressed, evolutionarily conserved gene encoding a predicted protein of 531 amino acids, for which we propose the name parafibromin. Our findings suggest that HRPT2 is a tumor-suppressor gene, the inactivation of which is directly involved in predisposition to HPT-JT and in development of some sporadic parathyroid tumors. 相似文献
169.
The C(2)B Ca(2+)-binding motif of synaptotagmin is required for synaptic transmission in vivo 总被引:6,自引:0,他引:6
Synaptotagmin is a synaptic vesicle protein that is postulated to be the Ca(2+) sensor for fast, evoked neurotransmitter release. Deleting the gene for synaptotagmin (syt(null)) strongly suppresses synaptic transmission in every species examined, showing that synaptotagmin is central in the synaptic vesicle cycle. The cytoplasmic region of synaptotagmin contains two C(2) domains, C(2)A and C(2)B. Five, highly conserved, acidic residues in both the C(2)A and C(2)B domains of synaptotagmin coordinate the binding of Ca(2+) ions, and biochemical studies have characterized several in vitro Ca(2+)-dependent interactions between synaptotagmin and other nerve terminal molecules. But there has been no direct evidence that any of the Ca(2+)-binding sites within synaptotagmin are required in vivo. Here we show that mutating two of the Ca(2+)-binding aspartate residues in the C(2)B domain (D(416,418)N in Drosophila) decreased evoked transmitter release by >95%, and decreased the apparent Ca(2+) affinity of evoked transmitter release. These studies show that the Ca(2+)-binding motif of the C(2)B domain of synaptotagmin is essential for synaptic transmission. 相似文献
170.
HIV-1 evades antibody-mediated neutralization through conformational masking of receptor-binding sites 总被引:54,自引:0,他引:54
Kwong PD Doyle ML Casper DJ Cicala C Leavitt SA Majeed S Steenbeke TD Venturi M Chaiken I Fung M Katinger H Parren PW Robinson J Van Ryk D Wang L Burton DR Freire E Wyatt R Sodroski J Hendrickson WA Arthos J 《Nature》2002,420(6916):678-682
The ability of human immunodeficiency virus (HIV-1) to persist and cause AIDS is dependent on its avoidance of antibody-mediated neutralization. The virus elicits abundant, envelope-directed antibodies that have little neutralization capacity. This lack of neutralization is paradoxical, given the functional conservation and exposure of receptor-binding sites on the gp120 envelope glycoprotein, which are larger than the typical antibody footprint and should therefore be accessible for antibody binding. Because gp120-receptor interactions involve conformational reorganization, we measured the entropies of binding for 20 gp120-reactive antibodies. Here we show that recognition by receptor-binding-site antibodies induces conformational change. Correlation with neutralization potency and analysis of receptor-antibody thermodynamic cycles suggested a receptor-binding-site 'conformational masking' mechanism of neutralization escape. To understand how such an escape mechanism would be compatible with virus-receptor interactions, we tested a soluble dodecameric receptor molecule and found that it neutralized primary HIV-1 isolates with great potency, showing that simultaneous binding of viral envelope glycoproteins by multiple receptors creates sufficient avidity to compensate for such masking. Because this solution is available for cell-surface receptors but not for most antibodies, conformational masking enables HIV-1 to maintain receptor binding and simultaneously to resist neutralization. 相似文献