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关注:1
2013-05-23 12:21
求翻译:Fibroblast growth factor receptors (Fgfrs) are expressed throughout the developing kidney. Several early studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud (UB). Transgenic mice that over-express a dominant negative receptor isoform develop renal aplasia/severe dysplasia, confirming the importance of Fgfrs in renal development. Furthermore, global deletion of Fgf7, Fgf10, and Fgfr2IIIb (isoform that binds Fgf7 and Fgf10) in mice leads to small kidneys with fewer collecting ducts and nephrons. Deletion of Fgfrl1, a receptor lacking intracellular signaling domains, causes severe renal dysgenesis. Conditional targeting of Fgf8 from the MM interrupts nephron formation. Deletion of Fgfr2 from the UB results in severe ureteric branching and stromal mesenchymal defects, although loss of Frs2α (major signaling adapter for Fgfrs) in the UB causes only mild renal hypoplasia. Deletion of both Fgfr1 and Fgfr2 in the MM results in renal aplasia with defects in MM formation and initial UB elongation and branching. Loss of Fgfr2 in the MM leads to many renal and urinary tract anomalies as well as vesicoureteral reflux. Thus, Fgfr signaling is critical for patterning of virtually all renal lineages at early and later stages of development.是什么意思?![]() ![]() Fibroblast growth factor receptors (Fgfrs) are expressed throughout the developing kidney. Several early studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud (UB). Transgenic mice that over-express a dominant negative receptor isoform develop renal aplasia/severe dysplasia, confirming the importance of Fgfrs in renal development. Furthermore, global deletion of Fgf7, Fgf10, and Fgfr2IIIb (isoform that binds Fgf7 and Fgf10) in mice leads to small kidneys with fewer collecting ducts and nephrons. Deletion of Fgfrl1, a receptor lacking intracellular signaling domains, causes severe renal dysgenesis. Conditional targeting of Fgf8 from the MM interrupts nephron formation. Deletion of Fgfr2 from the UB results in severe ureteric branching and stromal mesenchymal defects, although loss of Frs2α (major signaling adapter for Fgfrs) in the UB causes only mild renal hypoplasia. Deletion of both Fgfr1 and Fgfr2 in the MM results in renal aplasia with defects in MM formation and initial UB elongation and branching. Loss of Fgfr2 in the MM leads to many renal and urinary tract anomalies as well as vesicoureteral reflux. Thus, Fgfr signaling is critical for patterning of virtually all renal lineages at early and later stages of development.
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2013-05-23 12:26:38
碱性成纤维细胞生长因子受体 (Fgfrs) 来表示整个肾脏发育。早期的几项研究表明的增长和成熟的后肾间质 (毫米) 和输尿管芽 (优美),也将影响外源性碱性成纤维细胞生长因子 (Fgfs)。Over-express 显性负受体亚型的转基因小鼠发展肾发育不全/重度不典型增生,确认 Fgfrs 在肾脏发育中的重要性。此外,全球删除 Fgf7、 Fgf10 和 Fgfr2IIIb (绑定 Fgf7 和 Fgf10 的异构体) 在小鼠中会导致较少的收集的管道和 nephrons 的小肾脏。Fgfrl1,一种受体缺乏细胞内的信号转导域,删除导致严重肾发育不良。从 MM Fgf8 条件针对中断肾单位形成。从优美 Fgfr2 删除结果中重度输尿管分支和基质的间充质缺陷,虽然 Frs2α (主要为 Fgfrs 信号适配器) 损失优美的原因只有轻度肾发育不良。Fgfr1 和 Fgfr2 MM 中的删除导致 MM 形成和初始优美伸长和分支中的缺陷与肾发育不全。Fgfr2 MM 中损失导致许多肾功能及尿路异常,以及膀胱输尿管反流。因此,Fgfr 信号用于阵列的几乎所有肾宗族早期和后期阶段的发展至关重要。
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