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排序方式: 共有222条查询结果,搜索用时 15 毫秒
1.
Regional expression of the homeobox gene Nkx-2.2 in the developing mammalian forebrain. 总被引:11,自引:0,他引:11
M Price D Lazzaro T Pohl M G Mattei U Rüther J C Olivo D Duboule R Di Lauro 《Neuron》1992,8(2):241-255
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From the determination of the net and gross weight performed in the morning and at night the AA deduces that the normal growth of the chickens at night is inferior to that of the day time or directly negative. After fast the ingestion of food increases, therefore even night bodily growth is positive.--The fundamental factor of this recovery is due to hunger which is regulates by the hypothalamic centers. 相似文献
4.
Leberg Samuel S Barriga Ramiro Bart Henry Olivo Alfredo Narasimhan Kaushik Karubian Jordan 《Environmental Biology of Fishes》2021,104(3):239-251
Environmental Biology of Fishes - Environmental conditions influence ecological processes that shape stream community diversity and abundance. Deforestation has the potential to limit available... 相似文献
5.
Alessandro Pagliuso Thibault Lagache Roger Persson Audrey Salles Jean‐Christophe Olivo‐Marin Stéphane Oddos Anne Spang Pascale Cossart Fabrizia Stavru 《EMBO reports》2016,17(6):858-873
Mitochondria are essential eukaryotic organelles often forming intricate networks. The overall network morphology is determined by mitochondrial fusion and fission. Among the multiple mechanisms that appear to regulate mitochondrial fission, the ER and actin have recently been shown to play an important role by mediating mitochondrial constriction and promoting the action of a key fission factor, the dynamin‐like protein Drp1. Here, we report that the cytoskeletal component septin 2 is involved in Drp1‐dependent mitochondrial fission in mammalian cells. Septin 2 localizes to a subset of mitochondrial constrictions and directly binds Drp1, as shown by immunoprecipitation of the endogenous proteins and by pulldown assays with recombinant proteins. Depletion of septin 2 reduces Drp1 recruitment to mitochondria and results in hyperfused mitochondria and delayed FCCP‐induced fission. Strikingly, septin depletion also affects mitochondrial morphology in Caenorhabditis elegans, strongly suggesting that the role of septins in mitochondrial dynamics is evolutionarily conserved. 相似文献
6.
Jilmar A. Murillo Juan F. Gil Yulieth A. Upegui Adriana M. Restrepo Sara M. Robledo Winston Quiñones Fernando Echeverri Aurelio San Martin Horacio F. Olivo Gustavo Escobar 《Bioorganic & medicinal chemistry》2019,27(1):153-160
We describe the in vitro activity of two natural isomeric ent-beyerene diterpenes, several derivatives and synthetic intermediates. Beyerenols 1 and 2 showed EC50 of 4.6?±?9.4 and 5.3?±?9.4?μg/mL against amastigotes of L. (V) brazilensis, with SI of 5.1 and 7.7, respectively. Beyerenol 1 was synthesized from stevioside. In vivo experiments with bereyenols showed cure in 50% of hamsters infected with L. (V) brazilensis topically applied as Cream I (beyerenol 1, 0.81%, w/w) and Cream III (beyerenol 2, 1.96%, w/w). These results suggest that beyerenols are potential candidates for cutaneous leishmaniasis chemotherapy by topical application. In vitro assays of amastigotes of L. (V) brazilensis showed EC50 of 1.1?±?0.1 and 1.3?±?0.04?μg/mL, with SI of 3.1 and 3.5 for hydrazone intermediates 10 and 11, respectively. 相似文献
7.
Rac activation by lysophosphatidic acid LPA1 receptors through the guanine nucleotide exchange factor Tiam1 总被引:9,自引:0,他引:9
Van Leeuwen FN Olivo C Grivell S Giepmans BN Collard JG Moolenaar WH 《The Journal of biological chemistry》2003,278(1):400-406
Lysophosphatidic acid (LPA) is a serum-borne phospholipid that activates its own G protein-coupled receptors present in numerous cell types. In addition to stimulating cell proliferation, LPA also induces cytoskeletal changes and promotes cell migration in a RhoA- and Rac-dependent manner. Whereas RhoA is activated via Galpha(12/13)-linked Rho-specific guanine nucleotide exchange factors, it is unknown how LPA receptors may signal to Rac. Here we report that the prototypic LPA(1) receptor (previously named Edg2), when expressed in B103 neuroblastoma cells, mediates transient activation of RhoA and robust, prolonged activation of Rac leading to cell spreading, lamellipodia formation, and stimulation of cell migration. LPA-induced Rac activation is inhibited by pertussis toxin and requires phosphoinositide 3-kinase activity. Strikingly, LPA fails to activate Rac in cell types that lack the Rac-specific exchange factor Tiam1; however, enforced expression of Tiam1 restores LPA-induced Rac activation in those cells. Tiam1-deficient cells show enhanced RhoA activation, stress fiber formation, and cell rounding in response to LPA, consistent with Tiam1/Rac counteracting RhoA. We conclude that LPA(1) receptors couple to a G(i)-phosphoinositide 3-kinase-Tiam1 pathway to activate Rac, with consequent suppression of RhoA activity, and thereby stimulate cell spreading and motility. 相似文献
8.
B plexins activate Rho through PDZ-RhoGEF 总被引:3,自引:0,他引:3
Plexins are receptors for the repulsive axon guidance molecules semaphorins. Previously, we have shown that plexin-B1 binds activated Rac, but that clustering of plexin-B1 causes Rho activation, resulting in stress fiber formation. Using the yeast two-hybrid system, we found that the C-terminus of B plexins interacted directly with Rho-specific exchange factors, via their PDZ domain. Mutation of the carboxy-terminal amino acids of plexin-B1 or coexpression of a dominant negative PDZ-RhoGEF abrogated the ability of plexin-B1 to cause stress fiber formation. Our results demonstrate a role for PDZ-RhoGEF in B plexin-mediated activation of Rho/Rho kinase signaling, implicated in the regulation of axon guidance and cell migration. 相似文献
9.
Hilakivi-Clarke L Cabanes A Olivo S Kerr L Bouker KB Clarke R 《The Journal of steroid biochemistry and molecular biology》2002,80(2):163-174
The etiology of breast cancer is closely linked to the female hormone estrogen, with high life-time exposure being suggested to increase breast cancer risk [Nature 303 (1983) 767]. However, there appears to be a disparity between studies attempting to establish an association between high estrogen levels and breast cancer risk. This disparity becomes smaller by taking into consideration a timing factor, and we propose that estrogens can increase, decrease, or have no effect on breast cancer risk, depending on the timing of estrogen exposure. We further propose that the timing of estrogenic exposures may play at least as important a role in affecting breast cancer risk as life-time exposure. 相似文献
10.
van Beers JJ Raijmakers R Alexander LE Stammen-Vogelzangs J Lokate AM Heck AJ Schasfoort RB Pruijn GJ 《Arthritis research & therapy》2010,12(6):R219