首页> 外文期刊>Developmental dynamics: an official publication of the American Association of Anatomists >Time course of programmed cell death in Ciona intestinalis in relation to mitotic activity and MAPK signaling.
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Time course of programmed cell death in Ciona intestinalis in relation to mitotic activity and MAPK signaling.

机译:Ciona小肠中程序性细胞死亡与有丝分裂活性和MAPK信号传导有关的时程。

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Programmed cell death (PCD) in the ascidian species Ciona intestinalis (Tunicata; Chordata) is investigated from early larvae to juvenile stages, by means of digoxigenin-based terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) technique. At first, PCD in the swimming larva affects trunk mesenchyme and central nervous system (CNS), then it participates extensively to metamorphosis, until it is restricted to developing organs of juveniles. Analysis of patterns of cell death and division in the larval CNS question old models on the genesis of the adult C. intestinalis brain. Upon performing immunochemical and functional assays for mitogen-activated protein kinase (MAPK) kinase kinase-1 (MEKK1), MAPK kinase 1/2 (MEK1/2), c-Jun NH(2)-terminal kinase (JNK), and dual phosphorylated extracellular regulated kinase 1/2 (dpERK1/2), the neurogenic competence of the larval brain appears to rely on a combinatorial regulation of PCD by the mitogen-activated protein kinase signaling cascade. These results show that, in tunicates, PCD consists of a multistep program implicated in growth and patterning with various roles. Developmental Dynamics 230:251-262, 2004.
机译:通过基于洋地黄毒苷的末端脱氧核苷酸转移酶介导的生物素化UTP缺口末端标记(TUNEL)技术,研究了从早期幼虫到幼虫的海鞘物种Ciona intestinalis(Tunicata; Chordata)中的程序性细胞死亡(PCD)。首先,游泳幼虫中的PCD影响躯干间充质和中枢神经系统(CNS),然后广泛参与变态,直到局限于幼体发育器官。幼虫中枢神经系统细胞死亡和分裂的模式分析质疑成年梭状芽胞杆菌脑成因的旧模型。在执行针对丝裂原激活的蛋白激酶(MAPK)激酶激酶1(MEKK1),MAPK激酶1/2(MEK1 / 2),c-Jun NH(2)-末端激酶(JNK)和双重酶的免疫化学和功能分析磷酸化的细胞外调节激酶1/2(dpERK1 / 2),幼虫大脑的神经源性能力似乎依赖于丝裂素激活的蛋白激酶信号级联反应对PCD的组合调节。这些结果表明,在被膜中,PCD由涉及生长和构图的多步骤程序组成,并具有多种作用。发展动力学230:251-262,2004年。

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