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71.
Xiao D Palani A Sofolarides M Aslanian R West RE Williams SM Wu RL Hwa J Sondey C Lachowicz J Korfmacher WA 《Bioorganic & medicinal chemistry letters》2012,22(9):3354-3357
A structure-activity relationship study was undertaken to address the lack of oral exposure of the H3 antagonist 1, which incorporated an arylketone. Among a number of sub-series, the 4H-pyrido[1,2-a]pyrimidin-4-one analog 21 showed an improved PK profile in rat and mouse and was active in an obesity model. The pyrimidin-4-one proved to be a novel and useful ketone bioisostere. 相似文献
72.
Ting P Lee J Albanese M Tom W Solomon D Aslanian R Shih N West R 《Bioorganic & medicinal chemistry letters》2002,12(18):2643-2646
A novel non-imidazole fluorene oxime 1a has been identified as a histamine H(3) inhibitor, and its structure-activity relationship has been evaluated. 相似文献
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Claire L. Dovey Aaron Aslanian Sevil Sofueva John R. Yates Paul Russell 《DNA Repair》2009,8(12):1390-1399
Mms1 and Mms22 are subunits of an Rtt101-based E3 ubiquitin ligase required for replication of damaged DNA templates in Saccharomyces cerevisiae. The function and evolutionary conservation of this DNA repair module are unknown. Here we report the characterization of an Mms1 ortholog in Schizosaccharomyces pombe. Fission yeast Mms1 was discovered through its physical association with S. pombe Mms22 (also known as Mus7). Loss of S. pombe Mms1 results in the accumulation of spontaneous DNA damage, mitotic delay, and hypersensitivity to genotoxins such as camptothecin that perturb replisome progression. Homologous recombination repair proteins Rhp51 and Rad22 (Rad51 and Rad52 orthologs, respectively) are critical for survival in the absence of Mms1; however, there is no such requirement for Mus81–Eme1 Holliday junction resolvase that is essential for recovery from broken replication forks. Mms1 and Mms22 mutants share similar phenotypes and are genetically epistatic under unperturbed growth conditions and following exposure to genotoxins. From these data we conclude that an evolutionary conserved Mms1–Mms22 complex is required for replication of damaged DNA in fission yeast. 相似文献
77.
Pauline C. Ting Joe F. Lee Margaret M. Albanese Jie Wu Robert Aslanian Leonard Favreau Cymbelene Nardo Walter A. Korfmacher Robert E. West Shirley M. Williams John C. Anthes Maria A. Rivelli Michel R. Corboz John A. Hey 《Bioorganic & medicinal chemistry letters》2010,20(17):5004-5008
A structure–activity relationship study of the lead piperazinylcarbonylpiperidine compound 3 resulted in the identification of 4-benzimidazolyl-piperidinylcarbonyl-piperidine 6h as a histamine-3 (H3) receptor antagonist. Additional optimization of 6h led to the identification of compounds 11i–k with Ki ? 0.5 nM and good in vivo activity. 相似文献
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Dong Xiao Cheng Wang Anandan Palani Hon-Chung Tsui Gregory Reichard Sunil Paliwal Neng-Yang Shih Robert Aslanian Ruth Duffy Jean Lachowicz Geoffrey Varty Cynthia Morgan Fei Liu Amin Nomeir 《Bioorganic & medicinal chemistry letters》2010,20(21):6313-6315
Modification of prototype NK1 antagonist 2 resulted in the synthesis of a series of simple amides 6 and retroamides 9. These compounds were shown to be potent and orally active NK1 antagonists. 相似文献
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Roni Mamluk Irvith M Carvajal Brent A Morse Henry Wong Janette Abramowitz Sharon Aslanian Ai-Ching Lim Jochem Gokemeijer Michael J Storek Joonsoo Lee Michael Gosselin Martin C Wright Ray T Camphausen Jack Wang Yan Chen Kathy Miller Kerry Sanders Sarah Short Jeff Sperinde Gargi prasad Stephen Williams Robert Kerbel John ebos Anthony Mutsaers John D Mendlein Alan S Harris Eric S Furfine 《MABS-AUSTIN》2010,2(2):199-208
CT-322 is a new anti-angiogenic therapeutic agent based on an engineered variant of the tenth type III domain of human fibronectin, i.e., an Adnectin™, designed to inhibit vascular endothelial growth factor receptor (VEGFR)-2. This PE Gylated Adnectin was developed using an mRNA display technology. CT-322 bound human VEGFR-2 with high affinity (KD, 11 nM), but did not bind VEGFR-1 or VEGFR-3 at concentrations up to 100 nM, as determined by surface plasmon resonance studies. Western blot analysis showed that CT-322 blocked VEGF-induced phosphorylation of VEGFR-2 and mitogen-activated protein kinase in human umbilical vascular endothelial cells. CT-322 significantly inhibited the growth of human tumor xenograft models of colon carcinoma and glioblastoma at doses of 15–60 mg/kg administered 3 times/week. Anti-tumor effects of CT-322 were comparable to those of sorafenib or sunitinib, which inhibit multiple kinases, in a colon carcinoma xenograft model, although CT-322 caused less overt adverse effects than the kinase inhibitors. CT-322 also enhanced the anti-tumor activity of the chemotherapeutic agent temsirolimus in the colon carcinoma model. The high affinity and specificity of CT-322 binding to VEGFR-2 and its anti-tumor activities establish CT-322 as a promising anti-angiogenic therapeutic agent. Our results further suggest that Adnectins are an important new class of targeted biologics that can be developed as potential treatments for a wide variety of diseases.Key words: CT-322, adnectin, VEGFR-2, tumor angiogenesis, angiogenesis inhibitor, biologics, targeted therapy 相似文献
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