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91.
JIANG Jing AN Guoyong WANG Pengcheng WANG Pengtao HAN Jinfeng JIA Yanbin & SONG Chunpeng . College of Life Sciences Henan University Kaifeng China . College of Agriculture Science Henan Agriculture University Zheng-zhou China Correspondence should be addressed to Song Chunpeng 《科学通报(英文版)》2003,48(18):1919-1926
The plant hormone abscisic acid (ABA) is involved in regulating adverse physiological processes, including stomatal closure, seed development and germination, and mediating many environmental stress responses, such as drought, salinity and extreme temperatures[1,2]. In re-sponse to various stress stimuli, ABA synthesis is in-creased in plant cells, which triggers a series of physio-logical responses to adapt the stress conditions[1—3]. For example, under water deficit, ABA acts directly on… 相似文献
92.
Regulation of neutrophil apoptosis via death receptors 总被引:4,自引:0,他引:4
93.
A full-length calmodulin binding protein kinase cDNA ,AtCBK1 ,from Arabidopsis has been isolated by screening of an Arabidopsis cDNA library and by 5′-RACE-Northern blot and in situ hybridization indicated that the expression of AtCBK1 was more abundant in the vascular bundles and the meristems than in other tissues,The phylogenetic analyses revenl that AtCBK1 is different from animal CaMKs and it falls into CRK subgroup,indicating that they may come from different ancestors,The result suggests that AtCBK1 encoldes a CaM-binding serine/threonine protein kinase. 相似文献
94.
Wei Liang Chunzheng Yang Jing Qi Hui Peng Jianrong Duan Hanzhi Liu Dexian Zheng 《科学通报(英文版)》1998,43(14):1196-1196
In the present study, actions of phenothiazines(PTZ) in reversing multidrug resistance(MDR) and inhibiting PKC activity were investigated. It was found that the three PTZs caused 2.49, 36.58 and 75.78 fold reversal of K562/AO2 MDR cells resistant to adriamycin, respectively, while the chemosensitizer verapamil caused 40 fold reversal in the same condition, indicating that PTZ11 is a novel reversal agent of MDR and a potential chemotherapeutic reagent for tumor therapy. PKC activity analysis in the presence of PTZs showd that PTZ6 and PTZ11 inhibited rat brain protein kinase C activity in a manner of dose_dependent. The IC 50 values were (489.77±31.4) and (113±9.64) μmol/L, respectively. PTZ7 had no inhibition on PKC activity. Further study showed that PTZ11 could reduce PMA_mediated activation of PKC in a manner of dose_dependent, suggesting that PTZ11 might compete for the high_affinity phorbol ester binding site within PKC molecule. Recently, an X_ray structure of PMA in complex with PKC Cys2 activator_binding domain was solved. We therefore decided to explore the possible binding model of PTZ11 with PKC molecule using SYBYL 6.02 program. It was shown that the binding site of PTZ11 with PKC molecule partially overlapped with that of PMA, providing for the first time new data for designing PKC inhibitors and MDR reversal drugs. 相似文献
95.
T-cell signal transduction and the role of protein kinase C 总被引:3,自引:0,他引:3
The T lymphocyte has a vital part to play in maintaining the host response to bacterial and viral infection and also appears
to play a key pathological role in autoimmune diseases such as rheumatoid arthritis. In this review, we summarize the signalling
pathways which trigger antigen-driven T-cell proliferation and examine the evidence which suggests that protein kinase C (PKC)
is fundamental to this process. Finally, we discuss the therapeutic potential that PKC inhibitors may have in the treatment
of autoimmune disease.
Received 31 March 1998; received after revision 19 May 1998; accepted 19 May 1998 相似文献
96.
多肽生长因子(PGF)介导之信号的特异性.在于它们能与特殊的细胞表面受体相结合,激发细胞内的一系列生理生化过程.生长因子受体都具有内在的酪氨酸蛋白激酶(TPK)活性。生长因子与受体结合后能激活TPK,导致各种细胞蛋白质的磷酸化和受体自身的磷酸化.许多癌基因产物都具有TPK活性,TPK的功能是使生长因子信号变为细胞内信号。肿瘤细胞受体TPK区的突变体,虽然可能仍具有结合配体的能力,但丧失了刺激细胞内效应的能力。说明受体信号激活的关键是由一个功能性TPK决定的,并通过一些TPK的底物来介导细胞内的效应.这使人联想到肿瘤细胞之所以呈失控的增殖状态,与其受体TPK的激活及细胞蛋白磷酸化密切相关。 相似文献
97.
用改进的Kuby等人方法从大熊猫骨骼肌中纯化了肌酸激酶,并对此酶的某些性质进行了研究。纯化倍数为 35.7;收率17.3%;比活力为 55.3U/mg;等电点为 6.60。聚丙烯酰胺凝胶电泳鉴定为一条带。SDS聚丙烯酰胺凝胶电泳测得其亚基分子量为42 000,总分子量为 84 000,该酶是由两个相同亚基组成的二聚体。酶对肌酸的Km 为 5.26mmol/L;对ATP的 Km为 0.74mmol/L,酶的最适温度是 30~36℃;酶的最适pH大于8.0。 相似文献
98.
L. De Petrocellis V. Di Marzo G. Cimino 《Cellular and molecular life sciences : CMLS》1993,49(1):57-64
The participation of protein kinase C (PKC) in the regeneration of tentacles ofHydra vulgaris was studied. Regeneration was induced by 1,2-sn-dioctanoyl-glycerol (diC8) and the novel diterpenoidic diacylglycerol verrucosin B (VB), a potent PKC activator extracted from marine sources. VB substantially increasedHydra average tentacle number (ATN) at concentrations 10,000 times lower than those needed for diC8 to exert an analogous effect. When both synthetic and natural VB analogues were tested, the structure/activity relationship found inHydra tentacle regeneration was identical to that known for DAG-induced activation of PKC in vitro. VB-induced increase of ATN was strongly counteracted by the PKC inhibitors sphingosine and A3, but was not synergic with a tenfold increase of extracellular Ca2+ concentration or with an increase of intracellular Ca2+ concentration obtained either with the ionophore A23187 or with thapsigargin. This suggested the involvement of a non-Ca2+-dependent PKC in VB-triggeredHydra tentacle regeneration. The involvement of phospholipase A2 (PLA2) activation inHydra regenerative processes was studied using the novel site-specific inhibitor of the enzyme, oleyloxyethylphosphorylcholine (OOPC), which brought about a striking inhibition of ATN in the low molar range. This effect was reversed by arachidonic acid (AA), while an enhancement of ATN was also observed with an inhibitor of AA uptake from membrane phospholipids, thus suggesting that PLA2-catalysed liberation of AA is involved inHydra tentacle regeneration. OOPC also blocked verrucosin B-induced PKC-mediated enhancement of ATN, thus suggesting that this effect is also mediated by PLA2 activation. ATN was increased also by compound 48/80, a direct activator of pertussis toxin-sensitive GTP-binding proteins, and this effect was counteracted by pertussis toxin pretreatment. None of the known AA cascade inhibitors exhibited an effect on ATN comparable to that exerted by OOPC, but, surprisingly, the cycloxygenase inhibitor indomethacin strongly enhanced ATN, thus suggesting that prostanoids might effect a negative control onHydra regenerative processes. This represents the first attempt so far reported to study the implication of more than one biochemical pathway as a signalling event in the hydroid regenerative processes. 相似文献
99.
利用培养新生大鼠心肌细胞,检测NO前体L-精氨酸(L-arginine,L-Arg)和NO供体硝普钠(sodium nitroprusside,SNP)对PKC活性的影响,并探讨内、外源性NO在PKC激动剂佛波指(phorbol 12-myristate 13-acetate,PMA)激活PKC中的作用.实验结果表明:培养基中加入L-Arg,PKC活性呈剂量依赖性降低;用L-Arg进行预处理,30 min后加入PMA,PKC活性明显降低,与单纯PMA组相比有显著差异;NOS抑制剂L-NAME本身对基础状态PKC活性无明显影响,但可阻断L-Arg对上述2个效应的影响;培养液中加入NO供体SNP,PKC活性呈剂量依赖性降低;用SNP预处理心肌细胞,5 min后加入PMA,PKC活性与单纯PMA组相比有显著性差异.以上结果表明,内、外源性NO均具有剂量依赖性抑制PKC活性的作用,PKC可能是NO对心肌细胞作用的胞内信号传导通路的关键部位或重要信号分子之一;L-Arg通过NOS先生成NO,NO再对PKC起抑制作用. 相似文献
100.
To observe the regulation of platelet-derived growth factor (PDGF) receptor-βin myocyte stimulated by angiotensin II (AngII) at both integrated and cellular levels and reveal the signal transduction mechanism in cell, two kidneys, one clip (2K1C) renal hypertension were performed by placing a sliver clip around the left renal artery. Blood pressure and the ratio of left ventricular weight to body weight were measured at 4 and 8 weeks after operation. The content of AngII in heart was detected by radioimmunology assay; the protein level of PDGF receptor-βin heart was measured by Western blot analysis. The alteration of PDGF receptor-βstimulated by AngII and several inhibitors was observed on cultured neonatal rat ventricular myocyte (NRVM). The content of AngII in heart of 2K1C renal hypertensive rat at 4 and 8 weeks after operation was increased. Compared with sham group, 4 and 8 weeks after operation, PDGF receptor-βin heart of 2K1C group was upregulated by 100.3% and 127.1% (P < 0.05), respectively. This upregulation could be inhibited by captopril. For cultured myocyte, PDGF receptor-βwas increased by 47.1% after being stimulated by AngII and this upregulation could be inhibited by losartan which was an inhibitor of AT1 receptor. PLC inhibitor (U73122) and MEK inhibitor (PD98059) could partly inhibit PDGF receptor-βupregulation induced by AngII. These results suggested that AngII could upregulate PDGF receptor-βin myocyte by its AT1 receptor and this effect was at least partly dependent on PLC and extracellular signal-regulated kinase (ERK). 相似文献