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1.
细胞内游离Ca2+的荧光指示剂研究进展   总被引:1,自引:0,他引:1  
Ca2 在细胞的生命活动中起着重要作用,游离Ca2 浓度的变化与细胞的功能、信号传递及其损伤和凋亡都有着密切的联系,故胞内游离Ca2 浓度(简写为[Ca2 ]i)的含量及其时空分布的精确测定极为重要.对目前用于测定细胞内游离Ca2 浓度的常见荧光指示剂进行了综述,分析了常用的研究方法并对其优、缺点进行了简单的比较和评述.  相似文献   

2.
时丽冉 《生物学教学》2004,29(10):48-49
真核细胞内有数万种行使各种功能的蛋白质,在正常代谢条件下,蛋白质的合成和降解有精确的调节而处于动态平衡。内源性的蛋白质都有一定寿命,或长或短,最终命运是被降解。如果蛋白质的降解速率和位点出现异常,就会影响细胞的多种功能,如细胞分裂、信号传递等。目前发现真核细胞内有多条蛋白质降解途径,主要包括溶酶体途径、泛素一蛋白水解酶复合体通路、以及胱天蛋白酶(easpase)水解途径等。现简要介绍这几条途径。  相似文献   

3.
有丝分裂原活化蛋白激酶(MAPK)级联至少是由三种蛋白激酶组成的独特信号转导系统。MAPK级联介导细胞增殖和分化、细胞生长阻遏和凋亡。这些细胞信号酶把细胞外信号从细胞表面传递到细胞核,导致基因表达发生变化。信号转导级联的组分对肿瘤形成、免疫强化、炎症、伤口愈合和再生提供了新的治疗途径。  相似文献   

4.
PTP-1B是1988年被分离的一种蛋白质酪氨酸磷酸酶,它通过对胰岛素受体激酶活化部位(IRK)酪氨酸残基(pTyr)的去磷酸化来介导胰岛素信号.蛋白质酪氨酸磷酸化在信号转导的过程中起着关键作用,它通过在信号传导中的负调节功能导致个体胰岛素抵抗,从而发生糖脂代谢紊乱,进一步形成2型糖尿病.我国现有糖尿病患者约4000万,其中90%以上为2型糖尿病.21世纪2型糖尿病将成为中国、印度等亚太人口大国的流行病.随着对PTP-1B作用机理认识的逐渐深入,研究者发现它是2型糖尿病治疗的一个理想靶位点,为2型糖尿病发病机理和预防治疗研究提供了一条新的线索.该文综述了PTP-1B在基因结构、基因产物和生物学功能等方面的最新研究进展.  相似文献   

5.
本文从s wiss-prot中选取经过试验验证的水稻蛋白质磷酸化位点数据作为训练集合,应用蛋白质序列的氨基酸频率计算方法来进行特征提取,再利用SVM算法构建专门针对水稻蛋白质磷酸化位点的预测新工具.氨基酸频率算法指的是计算出相应待预测磷酸化位点附近氨基酸的出现频率,进一步反映了残基之间的相关性.本文利用LibSVM软件包对已通过氨基酸频率算法特征提取出来的数值特征对磷酸化位点进行预测,从而为之后构建水稻蛋白质磷酸化位点的预测工具做准备.结果表明,本文基于SVM和氨基酸频率方法的水稻蛋白质磷酸化位点预测在丝氨酸,苏氨酸和酪氨酸的平均预测准确性为77.665%,马修斯系数为0.571.与PlantPhos和Musite的预测性能的对比结果显示,在磷酸化苏氨酸位点的预测性能显著高于PlantPhos及Musite.  相似文献   

6.
钙/钙调素依赖性蛋白激酶Ⅱ是突触后致密成分的重要蛋白质组分,它能感受突触后钙离子水平的变化,并能通过自磷酸化维持长时活性,在调节谷氨酸能突触可塑性和学习记忆中有重要作用。  相似文献   

7.
胆碱乙酰化酶是乙酰胆碱的合成酶。胆碱乙酰化酶的磷酸化作用在胆碱能神经递质传递中起着重要的调控作用。蛋白激酶C异构体对胆碱乙酰化酶具有多级磷酸化作用;淀粉样肽也可调节胆碱乙酰化酶的磷酸化作用;含缬酪肽蛋白可能和磷酸化的胆碱乙酰化酶相互作用。  相似文献   

8.
细胞外信号调节蛋白激酶5(ERK5),也称大丝裂原活化蛋白激酶1,是ERK家族(MAPK大家族的一个亚家族)的一个重要成员。ERK5在背根神经节和脊髓中均有表达。本文着重阐述ERK5相关的信号通路在病理性疼痛中的作用:ERK5/CREB通路在疼痛信号的传递和痛觉过敏的形成中起重要作用;脊髓背角中ERK5的活化主要在小角质细胞;ERK5的活化可由NMDA受体介导。同时,我们细述了在病理性疼痛中,ERK5活化与NGF-TrkA和BDNF的关联。  相似文献   

9.
对家蚕中一未知基因进行生物信息学分析,结果显示:该基因开放阅读框大小为858 bp,编码285个氨基酸,预测分子量为31.1kD,等电点为4.75;该基因编码蛋白含有TPR(Tet ratrico Peptide Repeat)结构域,具有个蛋白激酶C磷酸化位点、酪蛋白激酶11磷酸化位点、肉豆蔻酰基化位点,糖基化位点及cAMP和cGMP依赖蛋白激酶磷酸化功能位点.  相似文献   

10.
植物体内活性氧代谢及功能研究进展   总被引:1,自引:0,他引:1  
最近生物化学和遗传学研究证明活性氧不仅仅是需氧生物细胞的代谢副产物,而且还是细胞内重要的信号分子,其中过氧化氢在介导植物体对生物和非生物胁迫响应中起一种信号分子作用。作为信号分子的活性氧有其特定的合成途径、专一性的代谢响应机制、专一性的作用靶标和信号调节完成之后的代谢消除途径。过氧化氢介导的信号调节作用包括ABA控制的气孔关闭、生长激素控制的根的向地性生长中、氧剥夺抗性的产生等。过氧化氢的合成和作用与一氧化氮有关系。过氧化氢调节的下游信号事件包括细胞内钙流动、蛋白质磷酸化和基因表达。钙和小G蛋白信号通路对于细胞内部过氧化氢的稳定状态维持具有重要作用。  相似文献   

11.
v-Src is a non-receptor protein tyrosine kinase involved in many signal transduction pathways and closely related to the activation and development of cancers. We present here the expression, purification, and bioactivity of a GST (glutathione S-transferase)-fused v-Src from a bacterial expression system. Different culture conditions were examined in an isopropyl ,B-D-thiogalactopyranoside (IPTG)-regulated expression, and the fused protein was purified using GSH (glutathione) affinity chromatography. ELISA (enzyme-linked immunosorbent assay) was employed to determine the phosphorylation kinase activity of the GST-fused v-Src. This strategy seems to be more promising than the insect cell system or other eukaryotic systems employed in earlier Src expression.  相似文献   

12.
钙离子作为胞内重要的第二信使,在细胞信号转导过程中发挥着极其重要的作用。探讨极低频电磁场对胞内游离钙离子浓度([Ca~(2 )]_i)的影响,对于从细胞信号转导的角度来解释生物电磁效应,尤其是弱极低频电磁场(ELF-EMF)非热效应的机制有着重要的意义。文章介绍了近年来有关极低频电磁场对胞内游离钙离子浓度影响的研究现状,并对今后的发展方向进行展望。  相似文献   

13.

The onset of inflammatory bowel disease (IBD) involves many factors, including environmental parameters, microorganisms, and the immune system. Although research on IBD continues to expand, the specific pathogenesis mechanism is still unclear. Protein modification refers to chemical modification after protein biosynthesis, also known as post-translational modification (PTM), which causes changes in the properties and functions of proteins. Since proteins can be modified in different ways, such as acetylation, methylation, and phosphorylation, the functions of proteins in different modified states will also be different. Transitions between different states of protein or changes in modification sites can regulate protein properties and functions. Such modifications like neddylation, sumoylation, glycosylation, and acetylation can activate or inhibit various signaling pathways (e.g., nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), and protein kinase B (AKT)) by changing the intestinal flora, regulating immune cells, modulating the release of cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ), and ultimately leading to the maintenance of the stability of the intestinal epithelial barrier. In this review, we focus on the current understanding of PTM and describe its regulatory role in the pathogenesis of IBD.

  相似文献   

14.
1.IntroductionInteractionsbetweenbonecellsandtheirextra-cellularmatrix(ECM)arecrucialinregulatingbonecellsadhesion,growth,migration,anddifferentiation.Amongtheseinteractions,thedirectcell-matrixattach-mentisthefundamentalofothercellbehaviors.BiochemicalandmechanicalsignalsfromtheECMcanbetransducedtocellinteriorviasomecell-surfacetransmembranereceptors.Severalfamiliesofreceptorsinvolvingintegrin,cadherin,selectinandimmuno-globulinsuperfamilyarerecognized.Recentstudieshavesuggestedthatintegri…  相似文献   

15.
Modification of proteins by phosphorylation is the major general mechanism by which many cellular functions in eukaryotic cells such as cell division, malignant transformation, differentiation, signal transduction etc. are controlled by external physiological stimuli. At the molecular level protein phosphorylation-dephosphorylation can alter various properties of the substrate molecules such as enzymatic activity, sub-Cellular location, ligand binding, interaction with other proteins, DNA binding and some other functional properties. The changes in molecular properties of proteins brought about by protein phosphorylation play a critical role in regulating various cellular functions.  相似文献   

16.
Bone morphogenetic proteins (BMPs) play a critical role in the growth and steroidogenesis of granulosa cells (GCs). BMP signals act through membrane-bound heteromeric serine/threonine kinase receptors. Upon ligand binding, BMPs activate intracellular Smad proteins and regulate growth and apoptosis in various cell types. The objective of this study was to demonstrate the effects of BMP/Smad signal on growth and steroidogenesis of porcine GCs. A strategy of RNA interference (RNAi)-mediated ‘gene silencing’ of Smad4, a core molecule mediating the intracellular BMP/Smad signal transduction pathways, was used to interrupt endogenous BMP/Smad signaling. Results indicate that Smad4-small interfering RNA (siRNA) caused specific inhibition of Smad4 mRNA and protein expression after transfection. Interrupted endogenous BMP/Smad signaling significantly inhibited growth, and induced apoptosis of porcine GCs, while decreasing estradiol production. In addition, interrupted BMP/Smad signaling significantly (P<0.05) changed the expression of Cyclin D2, CDK4, Bcl-2, and Cyp19a1. These findings provide new insights into how BMP/Smad signaling regulates the growth and steroidogenesis of porcine GCs.  相似文献   

17.
18.
Extracellular signal-regulated protein kinase 5 (ERK5), also known as big mitogen-activated protein kinase 1 (MAPK1), is an important member of ERK family, which is a subfamily of the large MAPK family. ERK5 is expressed in many tissues, including the dorsal root ganglion (DRG) neurons and the spinal cord. In this review, we focus on elaborating ERK5-associated pathway in pathological pain, in which the ERK5/CREB (cyclic adenosine monophosphate (cAMP)-response element-binding protein) pathway plays a crucial role in the transduction of pain signal and contributes to pain hypersensitivity. ERK5 activation in the spinal dorsal horn occurs mainly in microglia. The activation of ERK5 can be mediated by N-methyl-d-aspartate (NMDA) receptors. We also elaborate the relationship between ERK5 activation and nerve growth factor-tyrosine kinase A (NGF-TrkA), and the connection between ERK5 activation and brain-derived neurotrophic factor (BDNF) in pathological pain in detail.  相似文献   

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