...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Genetic Deletion of Murine SPRY Domain-Containing SOCS Box Protein 2 (SSB-2) Results in Very Mild Thrombocytopenia
【24h】

Genetic Deletion of Murine SPRY Domain-Containing SOCS Box Protein 2 (SSB-2) Results in Very Mild Thrombocytopenia

机译：小鼠SPRY域的SOCS框蛋白2（SSB-2）的基因删除导致非常轻度的血小板减少症。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The SSB family is comprised of four highly homologous proteins containing a C-terminal SOCS box motif and a central SPRY domain. No function has yet been ascribed to any member of this family in mammalian species despite a clear role for other SOCS proteins in negative regulation of cytokine signaling. To investigate its physiological role, the murine Ssb-2 gene was deleted by homologous recombination. SSB-2-deficient mice were shown to have a reduced rate of platelet production, resulting in very mild thrombocytopenia (25% decrease in circulating platelets). Tissue histology and other hematological parameters were normal, as was the majority of serum biochemistry, with the exception that blood urea nitrogen (BUN) levels were decreased in mice lacking SSB-2. Quantitative analysis of SSB mRNA levels indicated that SSB-1, -2, and -3 were ubiquitously expressed; however, SSB-4 was only expressed at very low levels. SSB-2 expression was observed in the kidney and in megakaryocytes, a finding consistent with the phenotype of mice lacking this gene. Deletion of SSB-2 thus perturbs the steady-state level of two tightly controlled homeostatic parameters and identifies a critical role for SSB-2 in regulating platelet production and BUN levels.
机译：SSB家族由四个高度同源的蛋白质组成，这些蛋白质包含一个C端SOCS盒基序和一个中央SPRY结构域。尽管其他SOCS蛋白在细胞因子信号转导的负调控中起着明显的作用，但尚未将此功能归因于哺乳动物中的该家族的任何成员。为了研究其生理作用，通过同源重组删除了小鼠 Ssb-2 基因。缺乏SSB-2的小鼠的血小板生成率降低，导致血小板减少症非常轻微（循环血小板减少25％）。组织病理学和其他血液学参数正常，大多数血清生化指标也正常，除了缺乏SSB-2的小鼠的血液尿素氮（BUN）水平降低外。对SSB mRNA水平的定量分析表明，SSB-1，-2和-3普遍存在。但是，SSB-4仅以非常低的水平表达。在肾脏和巨核细胞中观察到SSB-2表达，这一发现与缺乏该基因的小鼠的表型一致。因此，SSB-2的缺失会干扰两个严格控制的稳态参数的稳态水平，并确定SSB-2在调节血小板生成和BUN水平中的关键作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号