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mabaolin木虫 (正式写手)
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求干细胞几篇文章的摘要翻译
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1，题目：Homotypic signalling regulates Gata1 activity in the erythroblastic island 摘要： Gata1 is a transcription factor essential for erythropoiesis. Erythroid cells lacking Gata1 undergo apoptosis, while overexpression of Gata1 results in a block in erythroid differentiation. However, erythroid cells overexpressing Gata1 differentiate normally in vivo when in the presence of wild-type cells. We have proposed a model, whereby a signal generated by wild-type cells (red cell differentiation signal; REDS) overcomes the intrinsic defect in Gata1- overexpressing erythroid cells. The simplest interpretation of this model is that wild-type erythroid cells generate REDS. To substantiate this notion, we have exploited a tissue specific Cre/lox P system and the process of X- inactivation to generate mice that overexpress Gata1 in half the erythroid cells and are Gata1 null in the other half. The results show that the cells supplying REDS are erythroid cells. This study demonstrates the importance of intercellular signalling in regulating Gata1 activity and that this homotypic signalling between erythroid cells is crucial to normal differentiation. Key words: Erythropoiesis, Gata1, Homotypic signalling, REDS Summary 2，题目：Cooperation of Spi-1/PU.1 with an activated erythropoietin receptor inhibits apoptosis and Epo-Dependent differentiation in primary erythroblasts and induces their Kit ligand-dependent proliferation。 摘要 Spi-1/PU.1 is a myeloid –and B-cell specic transcrip-tion factor which is also involved in Friend virus-induced murine erythroleukemia.The pre-leukemic phase of Friend erythroleukemia results from activ-ation of the erythropoietin receptor(EpoR) by the spleen focus forming virus(SFFV) envelopeglyco-protein,followed by the emergence of leukemicclones characterized by over expression of Spi-1 and mutation of the p53 tumor suppress or gene. We developed a heterologous system to analyze the contribution of these alterations to the induction of primary erythroblast transformation. Avian erythroblasts expressing the activated mouse EpoR(R129C) differentiated into erythrocytes inresponse to hEpo. Expression of Spi-1 in these cells inhibited this ability to differentiate and rescued the cells from the apoptotic cell death program normally induced upon hEpo withdrawal. Although devoid of any effect by itself, a mutant p53 cooperated with Spi-1 and EpoR(R129C) to reinforce both pheno-types. Analysis of erythroblasts co-expressing Spi-1and the wild-type mouse EpoR showed that differentiation arrest and inhibition of apoptosis depended on specic cooperation between Spi-1 and EpoR(R129C). This cooperation was also required to induce the sustained proliferation of differentiation-blocked erythroblasts inresponse to ligand activation of the endogenous tyrosine kinase receptor c-Kit.These results show that Spi-1/PU.1 requires signals emanating from specic cytokine and growth factor receptors to affect the survival, proliferation and differentiation control of primary erythroblasts.They also suggest that the function of Spi-1/PU.1 in the late phase of Friend leukemia requires specic signaling from the gp55-modified EpoR gene rated during the early phase of the disease. Keywords :apoptosis/erythropoietinreceptor/Friend erythroleukemia/c-Kit/PU.1/Spi-1 3，题目Raf-1 Antagonizes Erythroid Differentiation by Restraining Caspase ctivation 摘要： The Raf kinases are key signal transducers activated by mitogens or oncogenes. The best studied Raf isoform, Raf-1, was identified as an inhibitor of apoptosis by conventional and conditional gene ablation in mice. c-raf-1 / embryos are growth retarded and anemic, and die at midgestation with anomalies in the placenta and fetal liver. Here, we show that Raf-1–deficient primary erythroblasts cannot be expanded in culture due to their accelerated differentiation into mature erythrocytes. In addition, Raf-1 expression is down-regulated in differentiating wild-type cells, whereas overexpression of activated Raf-1 delays differentiation. As recently described for human erythroid precursors, we find that caspase activation is necessary for the differentiation of murine fetal liver erythroblasts. Differentiation-associated caspase activation is accelerated in erythroid progenitors lacking Raf-1 and delayed by overexpression of the activated kinase. These results reveal an essential function of Raf-1 in erythropoiesis and demonstrate that the ability of Raf-1 to restrict caspase activation is biologically relevant in a context distinct from apoptosis. Key words: kinase . gene inactivation . erythropoiesis . fetal liver . apoptosis |
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