Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses

Jess M. Cunnick; Sabine Schmidhuber; Gang Chen; Min Yu; Sun-Ju Yi; Young Jin Cho; Vesa Kaartinen; Parviz Minoo; David Warburton; John Groffen; Nora Heisterkamp

首页> 外文期刊>Molecular and Cellular Biology >Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses

【24h】

Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses

机译：Bcr和Abr合作负调控急性炎症反应。

获取原文

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

Bcr and Abr are GTPase-activating proteins for the small GTPase Rac. Both proteins are expressed in cells of the innate immune system, including neutrophils and macrophages. The function of Bcr has been linked to the negative regulation of neutrophil reactive oxygen species (ROS) production, but the function of Abr in the innate immune system was unknown. Here, we report that mice lacking both proteins are severely affected in two models of experimental endotoxemia, including exposure to Escherichia coli lipopolysaccharide and polymicrobial sepsis, with extensive microvascular leakage, resulting in severe pulmonary edema and hemorrhage. Additionally, in vivo-activated neutrophils of abr and bcr null mutant mice produced excessive tissue-damaging myeloperoxidase (MPO), elastase, and ROS. Moreover, the secretion of the tissue metalloproteinase MMP9 by monocytes and ROS by elicited macrophages was abnormally high. In comparison, ROS production from bone marrow monocytes was not significantly different from that of controls, and the exocytosis of neutrophil secondary and tertiary granule products, including lactoferrin, was normal. These data show that Abr and Bcr normally curb very specific functions of mature tissue innate immune cells, and that each protein has distinct as well as partly overlapping functions in the downregulation of inflammatory processes.

机译：Bcr和Abr是小GTPase Rac的GTPase激活蛋白。两种蛋白均在先天免疫系统的细胞中表达，包括嗜中性粒细胞和巨噬细胞。 Bcr的功能已与嗜中性白细胞活性氧（ROS）产生的负调控相关联，但Abr在先天免疫系统中的功能尚不清楚。在这里，我们报告缺少两种蛋白质的小鼠在两种实验性内毒素血症模型中均受到严重影响，包括暴露于大肠埃希氏菌脂多糖和微生物败血症，并伴有大量微血管渗漏，从而导致严重的肺水肿和出血。此外，体内 abr 和 bcr 无效突变小鼠的嗜中性粒细胞产生了过量的破坏组织的髓过氧化物酶（MPO），弹性蛋白酶和ROS。此外，单核细胞分泌的组织金属蛋白酶MMP9和巨噬细胞分泌的ROS异常高。相比之下，从骨髓单核细胞产生的ROS与对照组无显着差异，并且嗜中性粒细胞二级和三级颗粒产品（包括乳铁蛋白）的胞吐作用正常。这些数据表明，Abr和Bcr通常会抑制成熟组织先天免疫细胞的非常特定的功能，并且每种蛋白质在炎症过程的下调中具有独特的以及部分重叠的功能。 展开▼

著录项

来源
《Molecular and Cellular Biology》 |2009年第21期|共9页

作者
Jess M. Cunnick; Sabine Schmidhuber; Gang Chen; Min Yu; Sun-Ju Yi; Young Jin Cho; Vesa Kaartinen; Parviz Minoo; David Warburton; John Groffen; Nora Heisterkamp;
展开▼

作者单位

展开▼

收录信息

原文格式 PDF

正文语种

中图分类细胞生物学;

关键词

相似文献

外文文献

中文文献

专利

1. Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses [J] . Jess M. Cunnick, Sabine Schmidhuber, Gang Chen, Molecular and Cellular Biology . 2009,第21期

机译：Bcr和Abr合作负调控急性炎症反应。

2. Zinc-binding protein-89 (ZBP-89) cooperates with NF-kappa B to regulate expression of matrix metalloproteinases (MMPs) in response to inflammatory cytokines [J] . Borghaei Ruth C., Gorski Grzegorz, Seutter Sara, Biochemical and Biophysical Research Communications . 2016,第4期

机译：锌结合蛋白89（ZBP-89）与NF-κB协同调节炎症反应因子对基质金属蛋白酶（MMP）的表达

3. Zinc-binding protein-89 (ZBP-89) cooperates with NF-kappa B to regulate expression of matrix metalloproteinases (MMPs) in response to inflammatory cytokines [J] . Borghaei Ruth C., Gorski Grzegorz, Seutter Sara, Biochemical and Biophysical Research Communications . 2016,第4期

机译：锌结合蛋白89（ZBP-89）与NF-κB协同调节炎症反应因子对基质金属蛋白酶（MMP）的表达

4. Modeling and Analysis of Acute Inflammatory Response Using Agent Based Approach [C] . Zhenzhen Shi, David Ben-Arieh, John Wu Annual Conference and Expo of the Institute of Industrial Engineers . 2014

机译：基于代理的方法急性炎症反应的建模与分析

5. Pax5 haploinsufficiency cooperates with BCR-ABL1 to induce acute lymphoblastic leukemia. [D] . Miller, Christopher B. 2009

机译：Pax5单倍体不足与BCR-ABL1协同诱导急性淋巴细胞白血病。

6. Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses [O] . Jess M. Cunnick, Sabine Schmidhuber, Gang Chen, 2009

机译：Bcr和Abr合作负调控急性炎症反应。

7. Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses▿ [O] . Cunnick, Jess M., Schmidhuber, Sabine, Chen, Gang, 2009

机译：Bcr和Abr合作消极调节急性炎症反应▿

1. 百草枯中毒急性炎症反应中Tim-3的调控作用研究 [J] . 于佳卉 ,沈倍奋 ,黎燕 . 军事医学 . 2016,第001期

2. 百草枯中毒急性炎症反应中Tim-3的调控作用研究 [J] . 于佳卉123 ,侯春梅1 ,蒋兴伟1 . 军事医学 . 2016,第001期

3. 细胞信号负调细胞信号负调控因子3调控Wnt/β-Catenin信号通路对肿瘤干细胞的影响及其在脑胶质母细胞瘤中的应用 [J] . 吴伟 . 中国组织工程研究 . 2012,第032期

4. ABR短潜伏期负波在前庭导水管扩大诊断上的价值 [J] . 舒毅 ,郭素英 . 中国医药指南 . 2013,第036期

5. 人EGFR显性负性突变体负调控内源性EGFR功能的机制分析 [J] . 廖刚 ,王子卫 ,赵林 . 生命科学研究 . 2010,第003期

6. TCRP1通过BCR-ABL和AKT1蛋白调控CML细胞的增殖 [C] . 刘孝荣 ,马东礼 ,陈小文 . 第二十次全国儿科中西医结合学术会议 . 2016

7. 布鲁氏菌胞质外σ因子bcrS系统调控抗氧化和毒力基因的机制及在致病过程中的作用 [A] . 李火明 . 2021

1. 降解高浓度高氯酸盐废水的ABR系统及调控方法 [P] . 中国专利： CN109133339B . 2021.05.18

2. 降解高浓度高氯酸盐废水的ABR系统及调控方法 [P] . 中国专利： CN109133339A . 2019-01-04

3. Processes to modulate the activity of knfb, to identify a compound or compounds capable of directly or indirectly modulating the activity of p105, to identify a reference compound for a pharmaceutical product usable in the treatment of disease involving or using an inflammatory response, identifiable compound antibody, polypeptide, and, processes to modulate p105 activity in a cell, use of a compound, to identify a compound that regulates an inflammatory response mediated by tpl-2, to identify a compound that regulates signal transduction by tpl-2, to identify a compound that modulates the interaction of a tpl-2 polypeptide with a target component of modulation of tpl-2, to treat an immune system condition in a patient in need of it by modulating tpl- activity 2, to treat a tpl-2-mediated condition in a patient, and to modulate tpl-2-mediated nfkb regulation in a patient in need hence, process to treat rheumatoid arthritis. [P] . 外国专利： BR9913070A . 2001-05-08

机译：调节knfb活性，鉴定能够直接或间接调节p105活性的化合物，鉴定可用于治疗涉及或使用炎症反应的疾病的药物的参考化合物的方法，多肽和调节细胞中p105活性的过程，使用化合物，鉴定调节tpl-2介导的炎症反应的化合物，鉴定调节tpl-2信号转导的化合物，鉴定通过调节tpl-活性2来调节tpl-2多肽与tpl-2调节靶标成分相互作用的化合物，以治疗有此需要的患者的免疫系统疾病，以治疗tpl-2介导的疾病因此，在需要治疗的患者中调节tpl-2介导的nfkb调节是治疗类风湿性关节炎的方法。

4. use of factor viia or a factor viia equivalent, parts kit and method to prevent or mitigate one or more late trauma complications, and methods to reduce the number of days a trauma patient is hospitalized after trauma to reduce the number of days a trauma patient spends in an intensive care unit after trauma, to improve lung function in a trauma patient, to reduce the risk of developing acute lung injury and / or acute respiratory distress syndrome in a patient. to reduce the risk of developing disseminated intravascular coagulation in a trauma patient, to reduce the risk of developing systemic inflammatory response syndrome in a trauma patient, to reduce the risk of developing multiple organ failure in a trauma patient , to reduce the risk of death in a trauma patient and to prevent or mitigate one or more late trauma complications. [P] . 外国专利： BRPI0507156A . 2007-06-26

机译：使用因子VIIa或因子VIIa等同物，预防或减轻一种或多种晚期创伤并发症的零件套件和方法，以及减少创伤后住院的创伤患者住院天数的方法，以减少创伤患者所花费的天数在创伤后的重症监护室中，以改善创伤患者的肺功能，降低患者发生急性肺损伤和/或急性呼吸窘迫综合征的风险。降低创伤患者发生弥散性血管内凝血的风险，降低创伤患者发生全身性炎症反应综合征的风险，降低创伤患者发生多器官衰竭的风险，降低死亡风险创伤患者，并预防或减轻一个或多个晚期创伤并发症。

5. Method for aligning derived-band ABR responses based on integration of detrended derived-band ABRs [P] . 外国专利： US7141022B1 . 2006-11-28

机译：基于去趋势化的衍生频带ABR的整合来对齐衍生频带ABR响应的方法

相关主题

Bcr and Abr Cooperate in Negatively Regulating Acute Inflammatory Responses

摘要

著录项

相似文献

相关主题

期刊订阅