Ask about this productRelated genes to: NRIP2 antibody
- Gene:
- NRIP2 NIH gene
- Name:
- nuclear receptor interacting protein 2
- Previous symbol:
- -
- Synonyms:
- DKFZP761G1913
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2014-11-19
Related products to: NRIP2 antibody
Related articles to: NRIP2 antibody
- Obesity is a significant risk factor for thoracic aortic dissection (TAD), as supported by UK Biobank data showing obese individuals have a higher risk of TAD. The study investigates leptin, a hormone elevated in obesity, and finds that hyperleptinemia is common in TAD patients, suggesting its role in disease pathogenesis. Using leptin-knockout mice, it is demonstrated that exogenous leptin exacerbates TAD by promoting phenotypic transitions in vascular smooth muscle cells (VSMCs). These adverse effects are reversible with pharmacologic leptin blockade, indicating potential therapeutic benefits. Single-cell RNA sequencing reveals a novel smooth muscle cells (SMC) cluster, Nrip2, in the aorta, with a distinct contractile gene profile. Increased Nrip2 VSMCs are linked to enhanced mitochondrial energy metabolism. Elevated Nrip2 VSMCs inhibit the leptin-induced transition from a contractile to a synthetic phenotype, reducing TAD incidence. The findings suggest that high blood leptin levels contribute to the increased TAD risk in obese individuals by suppressing Nrip2 SMCs, leading to abnormal mitochondrial metabolism and VSMC phenotypic transitions. Thus, targeting leptin to boost Nrip2 VSMC metabolic activity is a promising strategy for TAD prevention and treatment. - Source: PubMed
Publication date: 2025/07/16
Chen LingZhu YujieYang XiWu JiangBinChen KeyuanHuang WuqingFang LuZhang QiChen JieGao JianingCao HuanhuanWu MeifangQiu ZhihuangZhang YulingShen YueHuang QiuyuLin ZhiyongZheng LeminChen Liangwan - Limited success to date in development of drugs that target hallmark Alzheimer disease (AD) proteins as a means to slow AD-related cognitive decline has sparked interest in approaches focused on cognitive resilience. We sought to identify transcriptome signatures among brain donors with neuropathologically confirmed AD that distinguish those with cognitive impairment from those that were cognitively intact. - Source: PubMed
Publication date: 2024/11/13
Li DongheHan XudongFarrer Lindsay AStein Thor DJun Gyungah R - Colon adenocarcinoma (COAD) is one of the leading causes of death worldwide. Cancer stem cells (CSCs) are vital for COAD chemoresistance and recurrence, however little is known about stem cell-related biomarkers in drug resistance and COAD prognosis prediction. - Source: PubMed
Publication date: 2022/07/06
Li ZiyueChen JierongZhu DandanWang XiaoxiaoChen JaceZhang YuLian QizhouGu Bing - Activation of β-catenin causes podocyte injury and proteinuria, but how β-catenin signalling is regulated during podocyte injury remains elusive. Nuclear receptor interacting protein 2 (NRIP2) modulates the Wnt pathway in colorectal cancer-initiating cells, but the role of NRIP2 in podocyte injury has not yet been investigated. We aimed to examine the interaction between NRIP2 and β-catenin signalling. Knockdown or overexpression of NRIP2 and β-catenin and chemical treatments were performed in cultured human podocytes. Immunoprecipitation, immunoblotting and immunofluorescence assays were used to assess protein interactions and expression. Data from the GEO dataset and kidney tissues from patients with focal segmental glomerulosclerosis (FSGS) and surgical nephrectomy were examined. An adriamycin (ADR) nephropathy model was established in NRIP2 knockout mice. NRIP2 knockdown accelerated β-catenin degradation, which was reversed by MG132; specifically, NRIP2 bound β-catenin and stabilized it to prevent its degradation through the ubiquitin proteasomal pathway. Overexpression of NRIP2 led to β-catenin activation and Snail1 induction, and these effects were attenuated by β-catenin knockdown. NRIP2 knockdown blocked ADR-stimulated β-catenin activation. In ADR mice, genetic knockout of Nrip2 ameliorated podocyte injury and loss, glomerulosclerosis, and proteinuria by inhibiting β-catenin activation. Moreover, NRIP2 was significantly upregulated in podocytes of FSGS patients and colocalized with nuclear β-catenin. These results established NRIP2 as a stabilizer of β-catenin activation through the ubiquitin proteasomal pathway in podocyte injury. - Source: PubMed
Publication date: 2021/12/24
Hou QingLe WeiboKan ShuyanShi JinsongLang YueLiu ZhihongChen Zhaohong - Follicle-stimulating hormone (FSH) regulates ovarian follicular development through a specific gene expression program. We analyzed FSH-regulated transcriptome and histone modification in granulosa cells during follicular development. We used super-stimulated immature mice and collected granulosa cells before and 48 h after stimulation with equine chorionic gonadotropin (eCG). We profiled the transcriptome using RNA-sequencing (N = 3/time-point) and genome-wide trimethylation of lysine 4 of histone H3 (H3K4me3; an active transcription marker) using chromatin immunoprecipitation and sequencing (ChIP-Seq; N = 2/time-point). Across the mouse genome, 14,583 genes had an associated H3K4me3 peak and 63-66% of these peaks were observed within ≤1 kb promoter region. There were 72 genes with differential H3K4me3 modification at 48 h eCG (absolute log fold change > 1; false discovery rate [FDR] < 0.05) relative to 0 h eCG. Transcriptome data analysis showed 1463 differentially expressed genes at 48 h eCG (absolute log fold change > 1; FDR < 0.05). Among the 20 genes with differential expression and altered H3K4me3 modification, Lhcgr had higher H3K4me3 abundance and expression, while Nrip2 had lower H3K4me3 abundance and expression. Using ChIP-qPCR, we showed that FSH-regulated expression of Lhcgr, Cyp19a1, Nppc, and Nrip2 through regulation of H3K4me3 at their respective promoters. Transcript isoform analysis using Kallisto-Sleuth tool revealed 875 differentially expressed transcripts at 48 h eCG (b > 1; FDR < 0.05). Pathway analysis of RNA-seq data demonstrated that TGF-β signaling and steroidogenic pathways were regulated at 48 h eCG. Thus, FSH regulates gene expression in granulosa cells through multiple mechanisms namely altered H3K4me3 modification and inducing specific transcripts. These data form the basis for further studies investigating how these specific mechanisms regulate granulosa cell functions. - Source: PubMed
Publication date: 2020/09/06
Madogwe EjimedoTanwar Deepak KTaibi MilenaSchuermann YasminSt-Yves AudreyDuggavathi Raj