NFKBID

Last update 08 May 2025

Basic Info

Synonyms

I-kappa-B-delta, IkappaBdelta, IkappaBNS

+ [7]

Introduction

Regulates the expression of IL-2, IL-6, and other cytokines through regulation on NF-kappa-B activity. Functions in the regulation of inflammatory responses. Involved in the induction of T helper 17 cells (Th17) differentiation upon recognition of antigen by T cell antigen receptor (TCR). May also regulate TCR-induced negative selection of thymocytes.

100 Clinical Results associated with NFKBID

100 Translational Medicine associated with NFKBID

0 Patents (Medical) associated with NFKBID

Literatures (Medical) associated with NFKBID

21 Dec 2023·Journal of Virology

Hsa_circ_0007321 regulates Zika virus replication through miR-492/NFKBID/NF-κB signaling pathway

Article

Author: Jeyarajan, Andre J. ; Yang, Chunhui ; Ye, Haiyan ; Xu, Min ; Huang, Yike ; Warner, Charlotte A. ; Chen, Limin ; Li, Yujia ; Shi, Yaoqiang ; Duan, Xiaoqiong ; Kang, Lan ; Sun, Jujun ; Li, Shilin ; Xie, He ; Lin, Wenyu

ABSTRACTCircular RNAs (CircRNAs) have been shown to play a critical role in regulating viral infection and replication. We performed RNA sequencing to identify differentially expressed circRNAs in A549 human lung adenocarcinoma cells with and without Zika virus (ZIKV) infection. Notably, hsa_circ_0007321 was significantly downregulated after ZIKV infection. We then explored the role and mechanism of hsa_circ_0007321 in the regulation of ZIKV replication. Hsa_circ_0007321, derived from exons 2, 3, 4, and 5 of the DIS3L2 (DIS3 like 3'−5' exoribonuclease 2) gene, was mainly enriched in cytoplasm. We found that the knockdown of hsa_circ_0007321 significantly increased microRNA-492 levels to decrease NFKBID (NFKB inhibitor delta) expression, leading to the activation of the nuclear factor-κB (NF-κB) signaling pathway, inflammatory cytokine production, and subsequently, inhibition of ZIKV replication. These findings illustrate that hsa_circ_0007321 acts as a competitive endogenous RNA that regulates ZIKV replication through the miR-492/NFKBID NF-κB signaling pathway.IMPORTANCEOver the past decade, increasing evidence has shown that circular RNAs (circRNAs) play important regulatory roles in viral infection and host antiviral responses. However, reports on the role of circRNAs in Zika virus (ZIKV) infection are limited. In this study, we identified 45 differentially expressed circRNAs in ZIKV-infected A549 cells by RNA sequencing. We clarified that a downregulated circRNA, hsa_circ_0007321, regulates ZIKV replication through targeting of miR-492 and the downstream gene NFKBID. NFKBID is a negative regulator of nuclear factor-κB (NF-κB), and we found that inhibition of the NF-κB pathway promotes ZIKV replication. Therefore, this finding that hsa_circ_0007321 exerts its regulatory role on ZIKV replication through the miR-492/NFKBID/NF-κB signaling pathway has implications for the development of strategies to suppress ZIKV and possibly other viral infections.

07 Dec 2023·Blood

Oncogene-induced MALT1 protease activity drives posttranscriptional gene expression in malignant lymphomas

Article

Author: Grau, Michael ; Ober, Franziska ; Wimberger, Nicole ; Lenz, Georg ; Avar, Göksu ; Menden, Michael P ; Xu, Wendan ; Krappmann, Daniel

AbstractConstitutive mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) activity drives survival of malignant lymphomas addicted to chronic B-cell receptor signaling, oncogenic CARD11, or the API2-MALT1 (also BIRC3::MALT1) fusion oncoprotein. Although MALT1 scaffolding induces NF-κB–dependent survival signaling, MALT1 protease function is thought to augment NF-κB activation by cleaving signaling mediators and transcriptional regulators in B-cell lymphomas. However, the pathological role of MALT1 protease function in lymphomagenesis is not well understood. Here, we show that TRAF6 controls MALT1-dependent activation of NF-κB transcriptional responses but is dispensable for MALT1 protease activation driven by oncogenic CARD11. To uncouple enzymatic and nonenzymatic functions of MALT1, we analyzed TRAF6-dependent and -independent as well as MALT1 protease–dependent gene expression profiles downstream of oncogenic CARD11 and API2-MALT1. The data suggest that by cleaving and inactivating the RNA binding proteins Regnase-1 and Roquin-1/2, MALT1 protease induces posttranscriptional upregulation of many genes including NFKBIZ/IκBζ, NFKBID/IκBNS, and ZC3H12A/Regnase-1 in activated B-cell–like diffuse large B-cell lymphoma (ABC DLBCL). We demonstrate that oncogene-driven MALT1 activity in ABC DLBCL cells regulates NFKBIZ and NFKBID induction on an mRNA level via releasing a brake imposed by Regnase-1 and Roquin-1/2. Furthermore, MALT1 protease drives posttranscriptional gene induction in the context of the API2-MALT1 fusion created by the recurrent t(11;18)(q21;q21) translocation in MALT lymphoma. Thus, MALT1 paracaspase acts as a bifurcation point for enhancing transcriptional and posttranscriptional gene expression in malignant lymphomas. Moreover, the identification of MALT1 protease–selective target genes provides specific biomarkers for the clinical evaluation of MALT1 inhibitors.

01 Aug 2022·Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[Bioinformatics analysis of IκB gene family expression in human lung adenocarcinoma].

Article

Author: Yang, Jie ; Tang, Ming ; Xu, Wenfeng ; Yu, Hong ; Xie, Xiang ; Yuan, Qing

Objective To explore the clinical significance of inhibitor of NF-κB (IκB) family in lung adenocarcinoma (LUAD) through bioinformatics analysis. Methods The differentially expressed genes of IκB family in LUAD were screened by R language for survival analysis. The correlation between the expression of IκB family genes and clinicopathological characteristics was analyzed by R language, and the genes related to survival rate were selected for further study. GO and KEGG enrichment analyses were performed with LinkedOmics. The infiltration of immune cells was analyzed with TIMER. The correlation between the candidate genes and the prognosis of LUAD was analyzed through COX model. Results The expression levels of NF-κB inhibitor δ (NFKBID) and NF-κB inhibitor Zeta (NFKBIZ) were significantly downregulated in tumor tissues, and the patients with low expression levels of NFKBID and NFKBIZ had shorter overall survival. NFKBID and NFKBIZ were significantly correlated with T stage of LUAD. Enrichment analysis showed that low expression levels of NFKBID and NFKBIZ were correlated with energy metabolism and protein expression and transport. The expression levels of NFKBID and NFKBIZ were positively correlated with the infiltration of B cells, CD4⁺ T cells, neutrophils, and dendritic cells. COX analysis indicated that NFKBIZ could be an independent prognostic factor for LUAD. Conclusion The expression levels of NFKBID and NFKBIZ were significantly downregulated in tumor tissues, and were correlated with overall survival. NFKBID and NFKBIZ could be involved in the occurrence and development of LUAD by regulating glycometabolism and multiple immune cells infiltration. NFKBIZ could be considered as an independent prognostic factor for LUAD.

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