RIG-I is encoded by the DDX58 gene in humans. [9] [15] RIG-I is a helical ATP-dependent DExD/H box RNA helicase with a repressor domain (RD) on the C-terminus that binds to the target RNA.

2024年12月25日 · Among its related pathways are DDX58/IFIH1-mediated induction of interferon-alpha/beta and SARS-CoV-2 Infection. An important paralog of this gene is IFIH1 . UniProtKB/Swiss-Prot Summary for RIGI Gene

2019年9月21日 · 在人体中，对原发性黑色素瘤样本的转录组分析揭示出ddx58（编码rig-i的基因）的高表达、t细胞受体和抗原呈递途径活性与延长的总体存活期之间 ...

DDX58-201: 4621: 880aa: ENSP00000369212.1 . Gene/transcipt that contains an open reading frame (ORF). Protein coding. A2A376 O95786-A subset of the GENCODE transcript set, containing only 5' and 3' complete transcripts at protein-coding genes. GENCODE Basic, ENST00000379868.1: DDX58-002: 4089:

DDX58 and IFIH1 are members of the retinoic acid inducible-like receptors (RLR) and recognize exogenous RNA from many viruses, including coronavirus, Zika virus, and rubella. 7,9-11 DDX58 signals downstream through the mitochondrial activating complex, ultimately activating TANK-binding kinase (TBK1). 8 In turn, downstream phosphorylation of ...

Results: We have identified a novel DDX58 variant c.1529A>T p.(Glu510Val) that segregates with disease in two families with SGMRT2. Patients in these families have widely variable phenotypic features and different ethnic background, with some being severely affected by systemic features and others solely with glaucoma.

接着，作者进一步利用rnai和crispr-cas9技术构建了一系列基因敲低或敲除的细胞系来探究激活sting1的信号分子以及sting1如何激活自噬，鉴定出模式识别受体，即rna传感分子 rig-i （也称ddx58）能够将信号传递给sting1，另外结合免疫共沉淀，发现sting1通过与内质网膜 ...

2021年7月31日 · 为了探讨 rig-i 对 rig-i 配体诱导的肿瘤细胞死亡的影响，作者首先 利用 crispr-cas9 剪除人黑色素瘤细胞 1205lu 中表达 rig-i、mda5 以及 mavs 蛋白的基因(即 ddx58、ifih1 和 mavs)。

Results: We demonstrate a DDX58 autosomal dominant gain-of-function mutation, with constitutive upregulation of type I interferon. Conclusions: DDX58 mutations may be associated with the classic features of Singleton-Merten syndrome including dental dysplasia, tendon rupture, and severe cardiac sequela.

机制研究发现，ddx58 r109c突变可以解除rig-i蛋白自抑制，上调rig-i蛋白的k63泛素化水平，促进rig-i蛋白形成寡聚体，增强与下游mavs的相互作用，以及促进mavs聚集，从而激活rig-i-mavs介导的i型干扰素信号通路导致肾脏损害。