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RECS1(responsive to centrifugal force and shear stress gene 1)是一血液剪切力应答蛋白.RECS1基因敲除的小鼠年老时易患主动脉囊性中层坏死并表现有大动脉扩张症,暗示RECS1可能参与调控血管的发育重塑.免疫组化分析发现,RECS1基因敲除(RECS1 knockout,RECS1 KO)的小鼠主动脉基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)的表达水平明显提高,但RECS1的结构与功能及相关作用机理仍不清楚.研究发现,RECS1是肿瘤坏死因子受体2(tumor neucrosisfactor receptor 2,TNFR2)的结合蛋白质.报告基因检测实验表明,RECS1能特异地抑制TNFR2特异的激动性抗体或过量表达TNFR2诱导的核转录因子-κB(nuclear factor-κB,NF-κB)活化.NPLY模体缺失突变的RECS1不能结合TNFR2,并丧失对TNFR2介导NF-κB活化的抑制能力.稳定表达RECS1的MEFS细胞中,TNFR2特异的激动性抗体诱导的IκB(inhibitor of NF-κB)降解和NF-κB靶基因白介素-6(interleukin-6,IL-6)的表达均受到明显抑制.该研究揭示了RECS1通过与TNFR2的相互作用,负调控TNFR2介导肿瘤坏死因子信号传递的新功能及RECS1参与血管发育重塑调控的可能机制.
RECS1 (responsive to centrifugal force and shear stress gene 1) is a blood shear stress response protein.RECS1 knockout mice susceptible to age-related aortic cystic necrosis and the presence of aortic dilatation, suggesting RECS1 may be involved Regulate the development and remodeling of blood vessels.Immunohistochemical analysis showed that the expression of matrix metalloproteinase-9 (MMP-9) in RECS1 knockout (RECS1 KO) mice was significantly increased, However, the structure and function of RECS1 and its mechanism of action are not clear.Researches show that RECS1 is a binding protein of tumor necrosis factor receptor 2 (TNFR2) .Reporter gene test results show that RECS1 can specifically inhibit TNFR2-specific Activated or over-expressed TNFR2-induced nuclear factor-κB (NF-κB) activation.NRPLY mutant mutated RECS1 can not bind TNFR2, and loss of TNFR2-mediated inhibition of NF-κB activation The degradation of IκB induced by TNFR2-specific agonistic antibodies in MEFS cells stably expressing RECS1 and the degradation of NF-κB target gene interleukin-6 (IL-6) The study revealed that RECS1 negatively regulates TNFR2-mediated tumor necrosis factor signaling through its interaction with TNFR2, and RECS1 may be involved in the regulation of vascular remodeling.