Ask about this productRelated genes to: NRIP3 Blocking Peptide
- Gene:
- NRIP3 NIH gene
- Name:
- nuclear receptor interacting protein 3
- Previous symbol:
- C11orf14
- Synonyms:
- -
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-10-05
Related products to: NRIP3 Blocking Peptide
Related articles to: NRIP3 Blocking Peptide
- Cardiovascular disease (CVD) is a major cause of morbidity/mortality in juvenile-onset systemic lupus erythematosus (JSLE), yet no reliable tools exist to stratify CVD-risk. - Source: PubMed
Publication date: 2026/03/26
Peng JunjieDönnes PierreMcDonnell ThomasArdoin Stacy PSchanberg Laura ELewandowski Laura BJury Elizabeth CRobinson George ACiurtin Coziana - The KMT2A rearrangements is primarily caused by balanced translocations, with only a very small fraction resulting from deletions or inversions within the long arm of chromosome 11. - Source: PubMed
Publication date: 2025/10/31
Huang BingqingJia YujiaoQi BenquanWang HaoxuDuan ZhongchaoGuo XuXiao JigangSun QiZhu XiaofanXiao Zhijian - Genome-wide association studies have identified over 300 genomic loci associated with coronary artery disease (CAD) risk, but identifying functional variants remains challenging due to linkage disequilibrium. Here we show a comprehensive functional characterization of CAD-associated variants in primary vascular smooth muscle cells (SMCs). We performed lentivirus-based massively parallel reporter assays (lentiMPRAs) on 25,892 CAD-associated variants, testing their allele-specific enhancer activity in quiescent and proliferative SMCs. We identified 122 candidate variants with enhancer activity and allelic imbalance, including 23 variants showing condition-biased and 41 showing sex-biased effects. Integrating lentiMPRA with CUT&RUN epigenome profiling and expression quantitative trait loci data, we prioritized 49 functionally relevant variants. CRISPRi experiments on eight variants confirmed their regulatory effects on nine variant-gene pairs: rs35976034 (MAP1S), rs4888409 (CFDP1), rs73193808 (MAP3K7CL), rs67631072 (INPP5B/FHL3), rs1651285 (SNHG18), rs17293632 (SMAD3), rs2238792 (ARVCF) and rs4627080 (NRIP3). Our results fine-map the causal variants that confer CAD risk through their effects on vascular SMCs. - Source: PubMed
Publication date: 2025/10/07
Barbera NicolasLei LilyWallace AlexiaErin FarukPerry R Noahden Ruijter Hester MCivelek Mete - Epigenetic alterations critically affect tumor development. Polycomb-group complexes constitute an evolutionarily conserved epigenetic machinery that regulates stem cell fate and development. They are implicated in tumorigenesis, primarily via histone modification. Polycomb repressive complex 1 (PRC1) complexes 1-6 (PRC1.1-6) mediate the ubiquitination of histone H2A on lysine 119 (H2AK119ub). Here, we studied the functional roles of a PRC1.6 molecule, L3MBTL2, in neuroblastoma (NB) cells. L3MBTL2-knockout and knockdown revealed that L3MBTL2 depletion suppressed NB cell proliferation via cell-cycle arrest and gamma-H2A.X upregulation. L3MBTL2-knockout profoundly suppressed xenograft tumor formation. Transcriptome analysis revealed suppressed cell-cycle-related and activated differentiation-related pathways. Break repair meiotic recombinase recruitment factor 1 (BRME1) and nuclear receptor interacting protein 3 (NRIP3) were notably de-repressed by L3MBTL2-knockout. The deletion of L3MBTL2 reduced enrichment of H2AK119ub and PCGF6 at transcriptional start site proximal regions of the targets. Add-back studies unveiled the importance of L3MBTL2-BRME1 and -NRIP3 axes for NB cell proliferation. We further manifested the association of MYCN with de-repression of NRIP3 in an L3MBTL2-deficient context. Therefore, this study first revealed the significance of L3MBTL2-mediated gene silencing in MYCN-amplified NB cells. - Source: PubMed
Publication date: 2024/08/27
Okada RyuTakenobu HisanoriSatoh ShunpeiSugino Ryuichi POnuki RitsukoHaruta MasayukiMukae KyosukeNakazawa AtsukoAkter JesminOhira MikiKamijo Takehiko - Current prostate carcinoma (PCa) biomarkers, including total prostate-specific antigen (tPSA), have unsatisfactory diagnostic sensitivity and specificity resulting in overdiagnosis and overtreatment. Previously, we described an optimised bias-based preamplification-digital droplet PCR (OBBPA-ddPCR) technique, which detects tumour DNA in blood-derived cell-free DNA (cfDNA) of cancer patients. The current study investigated the performance of newly developed OBBPA-ddPCR-based biomarkers. Blood plasma samples from healthy individuals ( = 90, controls) and PCa ( = 39) and benign prostatic hyperplasia patients (BPH, = 40) were analysed. PCa and BPH patients had tPSA values within a diagnostic grey area of 2-15 ng/mL, for whom further diagnostic validation is most crucial. Methylation levels of biomarkers , , , and were found significantly increased in PCa patients compared to controls. By combining classical PCa risk factors (percentage of free PSA compared to tPSA (QfPSA) and patient's age) with cfDNA-based biomarkers, we developed PCa risk scores with improved sensitivity and specificity compared to established tPSA and QfPSA single-marker analyses. The diagnostic specificity was increased to 70% with 100% sensitivity for clinically significant PCa patients. Thus, prostate biopsies could be avoided for 28 out of 40 BPH patients. In conclusion, the newly developed risk scores may help to confirm the clinical decision and prevent unnecessary prostate biopsy. - Source: PubMed
Publication date: 2024/03/28
Friedemann MarkusJandeck CarstenTautz LarsGutewort Katharinavon Rein LisaSukocheva OlgaFuessel SusanneMenschikowski Mario