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排序方式: 共有645条查询结果,搜索用时 15 毫秒
1.
Ilham Bettahi David Pozo Carmen Osuna Russel J. Reiter Dario Acuña-Castroviejo Juan M. Guerrero 《Journal of pineal research》1996,20(4):205-210
Abstract: In this report, rat hypothalamic nitric oxide synthase (NOS) activity is shown to be partially inhibited by physiological concentrations of the pineal hormone melatonin. In vitro studies demonstrate that 1 nM melatonin, which approximates the physiological concentration of the hormone at night, significantly inhibited NOS activity. In vivo studies show that administering melatonin or collecting the hypothalamus from animals at night, when endogenous melatonin levels are elevated, results in a significant decrease of NOS activity. Results also show that calmodulin may be involved in this process since its presence in the incubation medium prevents the inhibitory effect of melatonin on NOS activity. 相似文献
2.
Injection of TFP (a specific antagonist of CaM) into the lateral ventricles of the rat brain on the fourth day of pregnancy causes marked antifertility effect in 83% of the rats (0% in the control group). Examination with the pontamone blue reaction for the implantation elucidated that the antifertitity effect was due to the blockage of implantation of the follicle. Injection of TFP into the lateral ventricles of the brain markedly reduced the concentration of CaM in hypothalamus, ovary and uterus. Serum progesterone was also reduced. However, injection glven on day 7 was ineffective to terminate the pregnancy. Injection given on certain time of pregnancy was able to reduce the cellular CaM content and to cause antifertitity. This finding demonstrated that CaM played an important rote during the course of pregnancy. 相似文献
3.
Fanasy P. Deming Ibtisam Al-Hashimi Nasser Haghighat William W. Hallmon David G. Kerns Celeste Abraham Francisco Rivera-Hidalgo 《Journal of oral pathology & medicine》2007,36(3):132-135
Background: Reduction in salivary secretion is the hallmark of Sjögren's syndrome (SS). Calmodulin (CaM) and calmodulin binding proteins (CaMBPs) play a key role in the secretory process of saliva. Recent studies have suggested that SS‐B, an autoantibody associated with SS, is a CaMBP. This finding suggests that CaMBP may contribute to the loss of saliva in SS. To better understand the role(s) of these proteins in SS, the purpose of this study was to compare salivary CaMBPs in Sjögren's patients and controls. Methods: Saliva samples were collected from 20 patients and 20 age‐, race‐, and gender‐matched controls. CaM overlay was used to identify CaMBPs in saliva of patients and controls. Results: Higher number of salivary CaMBPs was observed among patients than controls. Conclusions: The increased number of salivary CaMBPs in SS may suggest a potential role for these proteins in the pathogenesis of the disease. 相似文献
4.
目的:构建白念珠菌钙调蛋白基因(CMD1)缺陷HS3酵母菌体,为进一步探讨钙调蛋白基因突变对真菌生长周期及致病性的影响奠定基础。方法:首先将含cmd1::TRP1置换序列的质粒I转化二倍体酵母菌株YPH501(his3trplural),经Soutthern印迹法筛选出含TRP1序列的菌株。其次,将含CMD1序列的质粒Ⅱ转化以上TRP1阳性菌株,进行减数分裂后选择得到TRP1阳性酵母菌株单倍体。最后,将含trp1:HIS3置换序列质粒Ⅲ转化上述TRP1阳性单倍体菌株,用不含His培养基培养得到钙调蛋白基因缺陷HIS3酵母菌株。结果:经Southern印迹法证实cmd1:TRP1基因置换克隆;减数分裂后选择得到了TRP1阳性酵母菌株单倍体;质粒Ⅲ转化单倍体后经不含His培养基培养得到CMD1缺陷HIS3菌株,接种于不含Trp倍养基上未见有菌落生长,说明质粒Ⅲ转化单倍体后已将his3TRP1转换成HIS3trp1。结论:成功构建了钙调蛋白基因缺陷HIS3酵母菌株,基因型为cmd1trp1HIS3。 相似文献
5.
John Weaver Supatra Porasuphatana Pei Tsai Guan-Liang Cao Theodore A Budzichowski Linda J Roman Gerald M Rosen 《Toxicological sciences》2004,81(2):325-331
Neuronal nitric oxide synthase (NOS I) is a Ca(2+)/calmodulin-binding enzyme that generates nitric oxide (NO*) and L-citrulline from the oxidation of L-arginine, and superoxide (O(2)*(-)) from the one-electron reduction of oxygen (O(2)). Nitric oxide in particular has been implicated in many physiological processes, including vasodilator tone, hypertension, and the development and properties of neuronal function. Unlike Ca(2+), which is tightly regulated in the cell, many other divalent cations are unfettered and can compete for the four Ca(2+) binding sites on calmodulin. The results presented in this article survey the effects of various divalent metal ions on NOS I-mediated catalysis. As in the case of Ca(2+), we demonstrate that Ni(2+), Ba(2+), and Mn(2+) can activate NOS I to metabolize L-arginine to L-citrulline and NO*, and afford O(2)*(-) in the absence of L-arginine. In contrast, Cd(2+) did not activate NOS I to produce either NO* or O(2)*(-), and the combination of Ca(2+) and either Cd(2+), Ni(2+), or Mn(2+) inhibited enzyme activity. These interactions may initiate cellular toxicity by negatively affecting NOS I activity through production of NO*, O(2)*(-) and products derived from these free radicals. 相似文献
6.
INTRODUCTIONConstitutively expressed nitric oxide synthase(NOS) has three isoforms, including neuronal NOS(nNOS), inducible NOS (iNOS), and endothelial NOS(eNOS), which has been isolated and cloned[1]. NOScatalyzed L-arginine to generate L-citruline and nitricoxide (NO), a gaseous messenger molecule, the over-production of which plays a critical role in glutamate-induced neurotoxicity after ischemia[2]. In mutant micedeficient in nNOS and subsequent NO production, inf-arct s… 相似文献
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9.
Silvia G. Priori Andrea Mazzanti Demetrio J. Santiago Deni Kukavica Alessandro Trancuccio Jason C. Kovacic 《Journal of the American College of Cardiology》2021,77(20):2592-2612
In this final of a 5-part Focus Seminar series on precision medicine, we focus on catecholaminergic polymorphic ventricular tachycardia (CPVT). This focus on CPVT allows us to take a “deep dive” and explore the full extent of the precision medicine opportunities for a single cardiovascular condition at a level that was not possible in the preceding articles. As a new paradigm presented in this article, it has become clear that CPVT can occur as either a typical or atypical form. Although there is a degree of overlap between the typical and atypical forms, it is notable that they arise due to different underlying genetic changes, likely exhibiting differing mechanisms of action, and presenting with different phenotypic features. The recognition of these differing forms of CPVT and their different etiologies and mechanisms is an important step toward implementing rapidly emerging precision medicine approaches that will tailor novel therapies to specific gene defects. 相似文献
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