NFRKB

Last update 08 May 2025

Basic Info

Synonyms

DKFZp547B2013, DNA-binding protein R kappa-B, INO80 complex subunit G

+ [4]

Introduction

Binds to the DNA consensus sequence 5'-GGGGAATCTCC-3'. Putative regulatory component of the chromatin remodeling INO80 complex which is involved in transcriptional regulation, DNA replication and probably DNA repair. Modulates the deubiquitinase activity of UCHL5 in the INO80 complex.

100 Clinical Results associated with NFRKB

100 Translational Medicine associated with NFRKB

0 Patents (Medical) associated with NFRKB

693

Literatures (Medical) associated with NFRKB

01 Apr 2025·Modern Pathology

Cytogenomic and clinicopathological comparison of MYC-positive and MYC-negative High-grade B-cell lymphoma with 11q aberration in the context of other aggressive lymphomas with MYC rearrangement

Article

Author: Rymkiewicz, Grzegorz ; Ott, German ; Pienkowska-Grela, Barbara ; Grygalewicz, Beata ; Szafron, Laura A ; Woroniecka, Renata ; Horn, Heike ; Malawska, Natalia ; Szafron, Lukasz M ; Rygier, Jolanta ; Parada, Joanna ; Nowakowska, Beata ; Blachnio, Katarzyna ; Wojtkowska, Katarzyna ; Bystydzienski, Zbigniew

According to the 2022 WHO classification, High-grade B-cell lymphoma with 11q aberration (HGBCL-11q) is a MYC-negative lymphoma with 11q duplication and terminal deletion as specific chromosomal aberrations for this neoplasm. However, there are a growing number of reports defying this definition describing cases with the co-occurrence of 11q aberration and MYC rearrangement (HGBCL-11q,MYCR). This research has two aims. First, to compare the unique HGBCL-11q,MYCR group of 9 cases with 26 HGBCL-11q cases on chromosomal, mutational and clinicopathological level. The second objective is to investigate the association of the new HGBCL-11q,MYCR group with HGBCL-11q and two other closely related MYC-positive aggressive lymphoma subtypes: Burkitt lymphoma (BL) (n=17) and High-grade B-cell lymphoma, not otherwise specified with MYC rearrangement (n=10). Genetic results were obtained by classical cytogenetics, fluorescence in situ hybridization, microarrays, and whole exome sequencing. In parallel histopathological/ immunohistochemical analyses (HP/IHC) with flow cytometry(FCM), in conjunction with clinical presentation and treatment outcomes are presented. Our findings reveal that HGBCL-11q,MYCR, exists as an independent nosological entity, distinct from BL and HGBCL-11q at the cytogenetic, molecular, and clinicopathological levels, although it contains common features of both lymphoma subtypes. Common features with BL include: MYC rearrangement with the immunoglobulin genes, patterns of secondary chromosomal aberrations like dup(1q), del(17p), high number of MYC and CCND3 mutations. Other BL features are: frequent extranodal abdominal presentation, morphology, GCB cell of origin determined by IHC and FCM, immunophenotypical features such as MYC(+)/LMO2(-) detected by flow cytometric features: CD45(+)^weaker, more cases with CD43(+) and CD44(-) expression, only expression of IgD and IgM heavy chain and CD38(+)^higher overexpression, which correlates with MYC rearrangement assessed by FCM. Similarity to HGBCL-11q includes the existence of 11q aberration, presence of DDX3X, ETS1, GNA13, NFRKB, KMT2D, and the lack of TCF3 and ID3 mutations. Additionally, frequent nodal and tonsillar presentation, morphology, GCB cell of origin, immunophenotypical features with flow cytometry measured CD56(+) expression, associated with NCAM duplication/amplification on 11q, and pathogenesis not associated with Epstein-Barr virus infection. The distinctive chromosomal change of HGBCL-11q,MYCR was the gain or amplification of 3q29. Our cohort of patients with HGBCL-11q,MYCR had similar relapse-free survival to that of patients with HGBCL-11q and BL, if treated with BL-directed regimens.

01 Feb 2025·Advanced Science

Platelet–Monocyte Aggregate Instigates Inflammation and Vasculopathy in Kawasaki Disease

Article

Author: Jia, Cuiping ; Wang, Mengmeng ; Liu, Renjing ; Zhou, Jin ; Xie, Yinyin ; Wang, Ting ; Yarovinsky, Timur O. ; Tang, Wai Ho ; Guo, Manli ; Fu, Lanyan ; Gu, Xiaoqiong ; Jiang, Zhiyong ; Chen, Qian ; Hwa, John ; Che, Di ; Wen, Ying ; Edelson, Richard ; Zhang, Yuan ; Fan, Xuejiao ; Gao, Jingwen

AbstractKawasaki disease (KD) is a severe acute febrile illness and systemic vasculitis that causes coronary artery aneurysms in young children. Platelet hyperreactivity and an aberrant immune response are key indicators of KD; however, the mechanism by which hyperactive platelets contribute to inflammation and vasculopathy in KD remains unclear. A cytokine‐mediated positive feedback loop between KD platelets and monocytes is identified. KD platelet–monocyte aggregates (MPAs) are mediated by an initial interaction of P‐selectin (cluster of differentiation 62P, CD62p) and its glycoprotein ligand 1 (PSGL‐1). This is followed by a coordinated interaction of platelet glycoprotein (GP)Ibα with monocyte CD11b. Monocyte‐activated platelets initiate transforming growth factor (TGF)β1 release, which results in nuclear localization of nuclear factor kappaB in monocytes, therefore, driving the phenotypic conversion of classical monocytes (CD14+CD16−) into proinflammatory monocytes (CD14+CD16+). The platelet‐activated monocytes release interleukin‐1 and tissue necrotic factor‐α, which promote further platelet activation. KD‐induced inflammation and vasculopathy are prevented by inhibiting the components of this positive feedback loop. Notably, mice deficient in platelet TGFβ1 show less MPA and CD14+CD16+ monocytes, along with reduced inflammation and vasculopathy. These findings reveal that platelet–monocyte interactive proteins (CD62p/PSGL‐1 and (GP)Ibα/CD11b) and cytokine mediators (platelet TGFβ1) are potential biomarkers and therapeutic targets for KD vasculopathy.

01 Mar 2024·Journal of Hazardous Materials

An azole fungicide climbazole damages the gut-brain axis in the grass carp

Article

Author: Ma, Dong-Dong ; Shi, Wen-Jun ; Gao, Fang-Zhou ; Ying, Guang-Guo ; Long, Xiao-Bing ; Li, Si-Ying ; Zhang, Jin-Ge ; Zhang, Qian-Qian ; Lu, Zhi-Jie

Azole antifungal climbazole has frequently been detected in aquatic environments and shows various effects in fish. However, the underlying mechanism of toxicity through the gut-brain axis of climbazole is unclear. Here, we investigated the effects of climbazole at environmental concentrations on the microbiota-intestine-brain axis in grass carp via histopathological observation, gene expression and biochemical analyses, and high-throughput sequencing of the 16 S rRNA. Results showed that exposure to 0.2 to 20 μg/L climbazole for 42 days significantly disrupted gut microbiota and caused brain neurotoxicity in grass carp. In this study, there was an alteration in the phylum and genus compositions in the gut microbiota following climbazole treatment, including reducing Fusobacteria (e.g., Cetobacterium) and increasing Actinobacteria (e.g., Nocardia). Climbazole disrupted intestinal microbial abundance, leading to increased levels of lipopolysaccharide and tumor necrosis factor-alpha in the gut, serum, and brain. They passed through the impaired intestinal barrier into the circulation and caused the destruction of the blood-brain barrier through the gut-brain axis, allowing them into the brain. In the brain, climbazole activated the nuclear factor kappaB pathway to increase inflammation, and suppressed the E2-related factor 2 pathway to produce oxidative damage, resulting in apoptosis, which promoted neuroinflammation and neuronal death. Besides, our results suggested that this neurotoxicity was caused by the breakdown of the microbiota-gut-brain axis, mediated by reduced concentrations of dopamine, short chain fatty acids, and intestinal microbial activity induced by climbazole.

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