Ask about this productRelated genes to: RNF144B antibody
- Gene:
- RNF144B NIH gene
- Name:
- ring finger protein 144B
- Previous symbol:
- IBRDC2
- Synonyms:
- bA528A10.3, P53RFP
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-25
- Date modifiied:
- 2018-11-19
Related products to: RNF144B antibody
Related articles to: RNF144B antibody
- Chondrocalcinosis, characterized by calcium crystal deposition within articular cartilage, affects 5-15% of the general population and has recently been identified as an osteoarthritis risk factor. However, Its biological pathways remain unclear. We conducted a genome-wide association study of radiographically defined chondrocalcinosis knee and hand to identify its genetic determinants. - Source: PubMed
Publication date: 2026/08/20
Wu YahongXu YanningOkoro Paul CSaafi Sirinede Vries JardQi XiaoyiOei Edwin H GBierma-Zeinstra SitaVoortman TrudyFelson Davidvan Meurs Joyce BjChaker LayalWilkinson J MarkYau Michelle SBertrand JessicaBoer Cindy G - Major depressive disorder (MDD) is a prevalent mental illness, and inflammatory processes are considered a pivotal component of the pathogenesis of MDD. This study aims to identify novel biomarkers associated with the development of MDD and to elucidate the underlying immunological mechanisms. - Source: PubMed
Publication date: 2026/04/30
Wu XinyuZhou ShaomingYang PingChen JiayiLiu HonghuaShi LuZhang Xuehua - BACKGROUND: Myocardial infarction (MI) is a life-threatening cardiovascular disease characterized by high morbidity and mortality. Although advances in clinical management have improved patient outcomes, early diagnosis and effective immunomodulatory therapies remain limited. OBJECTIVE: This paper aims to identify key regulatory genes in MI, uncover their underlying mechanisms of action of the key genes, and facilitate their diagnostic and therapeutic use. METHODS: In this study, we integrated multiple transcriptomic datasets and applied machine learning approaches, including LASSO regression, to identify a robust 13 key genes significantly associated with MI. GSEA and GSVA were subsequently performed to explore their potential biological functions. The immunological relevance of these genes was evaluated by analyzing their correlations with inflammation-related genes and those involved in immune cell migration. In addition, transcription factor and microRNA (miRNA) regulatory networks were constructed to elucidate upstream regulatory mechanisms. The expression levels of the 13 key genes were validated in MI mouse model. RESULTS: Among 11 cardiac cell populations identified, myeloid cells contributed most prominently to MI pathogenesis. A robust 13-gene predictive signature was established, with RNF144B and C5AR1 showing strong associations with immune modulation and disease severity. Correlation analysis demonstrated a significant positive relationship of RNF144B and C5AR1 with immunological roles. TF-gene and miRNA–mRNA regulatory networks supported the post-transcriptional regulation of these genes. In the MI mouse model, expression of the 13 genes was consistent with the risk-prediction model. Molecular docking identified CCX168 as a promising small-molecule candidate targeting RNF144B and C5AR1. CONCLUSION: This study identified 13-gene signature, particularly RNF144B and C5AR1, holds promise as therapeutic targets, providing new insights for immunomodulatory and precision medicine strategies in MI. - Source: PubMed
Publication date: 2026/04/15
Hu YuxinChen LuSha JianmeiShao CaihongGao JunliYao Jianhua - Lung adenocarcinoma (LUAD) is a highly heterogeneous malignancy with poor clinical outcomes, underscoring the urgent need for robust prognostic biomarkers and therapeutically tractable regulatory molecules. Long non-coding RNAs (lncRNAs) have emerged as key modulators of tumor progression and immune regulation; however, the prognostic and functional significance of TMPO-AS1 in LUAD remains largely unexplored. - Source: PubMed
Publication date: 2026/04/13
Nirmal SakshiSaini ChainseeBaweja BhavikaVats PrernaPatidar PrachiJangir KritikaNema Rajeev - Stroke, as a predominant cerebrovascular event, is characterized by disproportionately high morbidity, disability, and mortality rates. The central role of neuroinflammation in its pathophysiology underscores the clinical significance of modulating related regulatory pathways. Notably, ring finger protein 144B (RNF144B), an E3 ubiquitin ligase with demonstrated anti-inflammatory properties, presents a potential novel therapeutic target. Herein, we aimed to rigorously investigate RNF144B's involvement in stroke pathogenesis and delineate its mechanistic underpinnings. RNF144B knockout (KO) and wild-type (WT) C57BL/6 male mice were subjected to middle cerebral artery occlusion (MCAO) to mimic ischemic stroke. Co-immunoprecipitation, immunofluorescent staining, western blot, RT-PCR were used to investigate the function and mechanism of RNF144B during MCAO. RNF144B expression was significantly upregulated following cerebral ischemic stroke. The absence of RNF144B promotes microglial activation and polarization, exacerbating neuroinflammatory responses. Mechanistically, RNF144B interacts with and promotes the K48-linked ubiquitination of Tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3), leading to its proteasomal degradation. The absence of RNF144B stabilizes TRAF3, thereby enhancing the activation of NF-κB and MAPK signaling pathways. Importantly, TRAF3 knockdown in RNF144B-deficient mice partially reversed the detrimental effects on neurological function, microglial activity, and neuroinflammation post-MCAO. The absence of RNF144B exacerbates stroke-induced neuroinflammation through TRAF3 stabilization, revealing this E3 ubiquitin ligase as a potential therapeutic target for cerebral ischemia. - Source: PubMed
Publication date: 2026/03/27
Hu DianboZhao ShuhuiJin YuetingYang ChenHu YugangLiu QianMa Renzheng