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1.
Growth hormone signal transduction 总被引:1,自引:0,他引:1
Growth hormone (GH) promotes animal growth by stimulating bone and cartilage cell proliferation, and influences carbohydrate and lipid metabolism. Some of these effects are brought about indirectly via somatomedin induction in hepatocytes, others by acting directly on the target cells. In either case, GH first binds to specific receptors on cells to trigger a sequence of biochemical events culminating in a biological response. Recently much has been learnt about the molecular structure of GH receptor, its binding to ligand, and the ensuing signal transduction events. 相似文献
2.
耳蜗的声感受是通过将大气压的微小波动转换成沿听神经传导的AP而实现的,HC在这-机-电换能过程中起关键作用。近二十年来,HC换能的生物物理特性研究取得许多重要突破,已在诸多方面从根本上改变了人们对听觉机制的传统认识。本文从HC换能模型、IHC与OHC的功能差异以及耳蜗声分析主动机制等三方面对这一领域进行了讨论与展望。 相似文献
3.
Colony-stimulating factor-1 (CSF-1), which is necessary for cell proliferation and differentiation, regulates both immediate
and delayed early responses throughout G1 phase. The binding of CSF-1 to its receptor (CSF-1R) triggers phosphorylation of
the receptor and its intrinsic tyrosine kinase. The activated receptor binds directly to cytoplasmic effector proteins, which
induce multiple-signal transduction pathways. CSF-1 can induce the c-myc gene expression via Ras and Ets-related proteins.
The expression of c-fos/jun family genes is also targeted following the activation of Ras. CSF-1R activates STAT1 and STAT3
to participate in signaling, but JAKs do not appear to contribute to signaling by CSF-1R. CSF-1R activates PI3-kinase, and
PI3-ki can interact with downstream proteins by the MAPKK-related pathway independent of Ras/Raf. PC-PLC can enforce signaling
in response to CSF-1. Furthermore, the turnover and dephosphorylation by the phosphatase SHPTP1 of CSF-1R are the major mechanism
in the negative regulation of signaling by CSF-1R 相似文献
4.
发展并建立了用于快速联合检测O2和CO2气体的调制电位脉冲微库仑法.对在非水电化学体系中实现两者一次检测的实时动态传感技术进行了系统研究.结果表明,这一新的电化学传感技术可望用来实时监测生物呼吸代谢过程中O2和CO2气体分压的动态变化 相似文献
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ZHENG Min WANG Dongmei HOU Lingling LI Haimin XIE Chao JIAO Wencang BAI Cixian WANG Yaping PEI Xuetao 《自然科学进展(英文版)》2004,14(1):26-30
Ascorbic acid (AA) induced differentiation of neural stem cells (NSCs) into dopaminergic (DAergic) neurons is reported.NSCs derived from rat mesencephalon were maintained and expanded in a defined medium containing mitogens of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF).Compared with the control, ascorbic acid treatment led to more DAergic neuronal differentiation as indicated by the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT), which are specific markers of dopamine neurons.AA induction also enhanced expression of Nurr1 and Shh.PD98059, an inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, could block AA-induced Nurr1, TH and DAT mRNA expression.The results might suggest a new strategy to provide enough dopaminergic cells for the therapy of Parkinson's disease (PD), and Nurr1 and ERK signaling pathway might participate in the AA-induced DAergic differentiation. 相似文献
8.
Identification of rate-limiting steps or components of intracellular second messenger systems holds promise to effectively
interfere with these pathways under pathological conditions. The emerging literature on a recently identified family of signalling
regulator proteins, called tribbles gives interesting clues for how these proteins seem to link several ‘independent’ signal
processing systems together. Via their unique way of action, tribbles co-ordinate the activation and suppression of the various
interacting signalling pathways and therefore appear to be key in determining cell fate while responding to environmental
challenges. This review summarises our current understanding of tribbles function and also provides an evolutionary perspective
on the various tribbles genes.
Received 10 January 2006; received after revision 20 March 2006; accepted 5 April 2006 相似文献
9.
Pahan K 《Cellular and molecular life sciences : CMLS》2006,63(10):1165-1178
Although a change in life-style is often the method of first choice for lipid lowering, lipid-lowering drugs, in general,
help to control elevated levels of different forms of lipids in patients with hyperlipidemia. While one group of drugs, statins,
lowers cholesterol, the other group, fibrates, is known to take care of fatty acids and triglycerides. In addition, other
drugs, such as ezetimibe, colesevelam, torcetrapib, avasimibe, implitapide, and niacin are also being considered to manage
hyperlipidemia. As lipids are very critical for cardiovascular diseases, these drugs reduce fatal and nonfatal cardiovascular
abnormalities in the general population. However, a number of recent studies indicate that apart from their lipidlowering
activities, statins and fibrates exhibit multiple functions to modulate intracellular signaling pathways, inhibit inflammation,
suppress the production of reactive oxygen species, and modulate T cell activity. Therefore, nowadays, these drugs are being
considered as possible therapeutics for several forms of human disorders including cancer, autoimmunity, inflammation, and
neurodegeneration. Here I discuss these applications in the light of newly discovered modes of action of these drugs.
Received 5 September 2005; received after revision 29 December 2005; accepted 26 January 2006 相似文献
10.
Src-family kinases (SFKs) regulate different granulocyte and monocyte/macrophage responses. Accumulating evidence suggests that members of this family are implicated in signal transduction pathways regulating phagocytic cell migration and recruitment into inflammatory sites. Macrophages with a genetic deficiency of SFKs display marked alterations in cytoskeleton dynamics, polarization and migration. This same phenotype is found in cells with either a lack of SFK substrates and/or interacting proteins such as Pyk2/FAK, c-Cbl and p190RhoGAP. Notably, SFKs and their downstream targets also regulate monocyte recruitment into inflammatory sites. Depending on the type of assay used, neutrophil migration in vitro may be either dependent on or independent of SFKs. Also neutrophil recruitment in in vivo models of inflammation may be regulated differently by SFKs depending on the tissue involved. In this review we will discuss possible mechanisms by which SFKs may regulate phagocytic cell migratory abilities. 相似文献