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The pro-survival Bcl-2 family member A1 delays spontaneous and FAS ligand-induced apoptosis of activated neutrophils

机译:Pro-survival bcl-2家族成员A1延迟自发性和Fas配体诱导的活性中性粒细胞的凋亡

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Neutrophils have a short lifespan that is extended after exposure to granulocyte macrophage colony stimulating factor (GM-CSF) or lipopolysaccharide (LPS)1 . While the survival is regulated by BCL-2 family proteins2 , it is not known which pro-survival proteins are involved. GM-CSF stimulation in neutrophils upregulates A1, but A1-defi- cient mice showed no defects in this cell type3 . MCL-1 is critical for the survival of quiescent neutrophils4,5 , but it is not known whether the same holds true after activation. We hypothesized that A1 and MCL-1 have overlapping roles in the survival of activated neutrophils.
机译:中性粒细胞在暴露于粒细胞巨噬细胞群刺激因子(GM-CSF)或脂多糖(LPS)1后延长延长的寿命短。虽然生存率由BCL-2家族蛋白质2调节,但尚未知道涉及哪种蛋白质蛋白质。 GM-CSF在中性粒细胞上促上α1,但A1分析小鼠在该细胞中没有显示出缺陷3。 MCL-1对于静态中性粒细胞4,5的存活至关重要,但是在激活后,尚不知道是否相同的保持真实。我们假设A1和MCL-1在活化中性粒细胞的存活中具有重叠的作用。

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