MAPRE3 (aa151_164)
- Known as:
- MAPRE3 (aa151_164)
- Catalog number:
- Y214453
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MAPRE3 (aa151_164)
Related genes to: MAPRE3 (aa151_164)
- Gene:
- MAPRE3 NIH gene
- Name:
- microtubule associated protein RP/EB family member 3
- Previous symbol:
- -
- Synonyms:
- RP3, EB3
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-10-05
Related products to: MAPRE3 (aa151_164)
Related articles to: MAPRE3 (aa151_164)
- The MAPRE3 gene is aberrantly expressed in several cancers. We profiled DNA methylation in tumor tissues from early-stage non-small cell lung cancer (NSCLC) patients and assessed associations with overall survival (OS). Significant CpG probes were validated in The Cancer Genome Atlas (TCGA). The methylation level of cg12821679 showed significant associations with OS in lung squamous cell carcinoma (LUSC) (HR = 0.32, P = 6.55 × 10), but it was not observed in lung adenocarcinoma (LUAD). In LUSC, MAPRE3 expression was significantly correlated with cg12821679 (r = 0.17, P = 2.96 × 10) and potential trans-regulated genes were enriched in the Nicotine addiction pathway. Additionally, MAPRE3 expression showed significant associations with OS in both LUAD and LUSC (LUAD: HR = 2.28, P = 2.40 × 10; LUSC: HR = 1.61, P = 0.0244). The association between smoking cessation and overall survival was significantly modified by MAPRE3 expression (HR = 0.69, P = 0.0282). Smoking cessation improved OS only in patients with high MAPRE3 expression (HR = 0.56, P = 2.82 × 10). We conclude MAPRE3 may predict NSCLC prognosis and influence the prognostic benefit of smoking cessation. - Source: PubMed
Publication date: 2026/04/25
Chen ChaoCheng JianchengHou RuiliZheng XiaoyuanSu LiBjaanæs Maria MoksnesKarlsson AnnaPlanck MariaStaaf JohanHelland ÅslaugEsteller ManelChristiani David CChen FengCao XiaofeiZhang Ruyang - Rapidly progressive Alzheimer's disease (rpAD) is a rare subtype with rapid decline, but its molecular underpinnings remain poorly defined. Here, brain-derived tau oligomers (TauO) were systematically compared across nondemented controls, slowly progressive AD (spAD), and rpAD to test whether subtype-specific TauO signatures align with clinical aggressiveness. TauO were immunoprecipitated from frontal cortex using T22 antibody and characterized by Western blotting, transmission electron microscopy, label-free quantitative proteomics, and SH-SY5Y toxicity assays, complemented by longitudinal analysis of tau phosphorylation in inoculated 3xTg AD mice. T22-positive high-molecular-weight TauO were successfully enriched from all groups, where rpAD TauO exhibited compact, densely packed oligomers under TEM and the highest phosphorylation at pS396 and pS422, exceeding both spAD and controls (p ≤ 0.0327). In 3xTg mice, pS396 showed an early increase followed by a late decline, consistent with dynamic shifts in tau solubility during disease evolution. Brain-derived TauO from spAD and rpAD, but not recombinant tau monomers or control-derived TauO, significantly reduced SH-SY5Y cell viability. Proteomic profiling identified 2388 TauO-associated proteins, including a shared 556-protein core and a striking expansion of rpAD-unique interactors (n = 1101). In controls and spAD, the core TauO interactome was enriched for translation, proteostasis, mitochondrial respiration, and vesicle-trafficking pathways, whereas these modules were absent in rpAD. Instead, rpAD TauO showed selective enrichment of aldehyde detoxification, amino-acid and carbon metabolism, and actin-regulatory modules, alongside increased association of SERPINA1, ALDH9A1, MAPRE3, DPYSL2, DPYSL3, and NFASC and reduced coupling to mitochondrial (MRPL17) and complement (C9) components. These convergent structural, post-translational, toxic, and interactome changes indicate that rpAD is defined by a biochemically distinct TauO species embedded in a metabolic and cytoskeleton-focused network, providing a mechanistic framework for its aggressive clinical course and a basis for subtype-specific biomarker and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/18
Saleem TayyabaMöbius WiebkeSchmitz Matthiasda Silva Correia AngelaThomas CarolinaCanaslan SezgiHermann PeterGöbel StefanZafar SaimaRoot ElisabethStadelmann ChristineAndreoletti OlivierHoppert MichaelFleming Outeiro TiagoFerrer IsidreYounas NeelamZerr Inga - The glymphatic system plays a key role in brain waste clearance, but its genetic regulation remains poorly understood. Diffusion Tensor Image Analysis along the Perivascular Space (DTI-ALPS) index is a non-invasive imaging biomarker to asses glymphatic system activity. We integrated mean DTI-ALPS genome-wide association study (GWAS) data from 31,021 individuals of European ancestry with GTEx v8 multi-tissue eQTL data to perform transcriptome-wide association studies (TWAS) using Unified Test for Molecular Signature (UTMOST) and Functional Summary-based Imputation (FUSION). Gene-level associations were further validated by Multi-marker Analysis of Genomic Annotation (MAGMA). Causal inference was conducted using cis-Mendelian randomization (cis-MR) and summary-data-based Mendelian randomization (SMR), while colocalization was applied to provide evidence of strong associations between two traits within a single genetic region, thereby ensuring the stability of the MR conclusions. TWAS identified 17 candidate genes (AGBL5-IT1, CENPA, CGREF1, DNAJC5G, EMILIN1, GCAT, KHK, MAPRE3, OTOF, PLCL1, PREB, RBM43, RFTN2, SERPIND1, SNAP29, TRIOBP, and UCN), among which six protein-coding genes (TRIOBP, MAPRE3, EMILIN1, KHK, GCAT, and CGREF1) were further validated by MAGMA. Cis-MR provided evidence for the causal effects of these six genes, while colocalization supported that the MR conclusions were stable for four of them (TRIOBP, MAPRE3, EMILIN1, and GCAT). Finally, SMR identified three genes (TRIOBP, GCAT, and MAPRE3) that showed consistent and robust associations with DTI-ALPS across multiple tissues. These findings provide statistical evidence for genetic regulation of glymphatic function. - Source: PubMed
Publication date: 2025/12/05
Zhu XiaoyangWang ShengjieZhang ShuaiqiLiu ZhiyuanWang NaWang ShuYang Nixia - Intervertebral disc degeneration (IDD) is a prevalent spinal condition frequently associated with pain and motor impairment, imposing a substantial burden on quality of life. Despite extensive investigations into the genetic predisposition to IDD, the precise pathogenic genes and molecular pathways involved remain inadequately characterized, underscoring the need for continued research to clarify its genetic underpinnings. - Source: PubMed
Publication date: 2025/09/07
Zhang LiZhao WenYang HongshengDeng TingtingLi Yugang - Biliary atresia (BA) is a rare pediatric cholestatic disorder characterized by progressive bile duct inflammation and fibrosis. The underlying molecular mechanisms of BA remain poorly defined. This study aimed to identify susceptibility genes causally associated with BA by integrating genome-wide association study (GWAS) and transcriptomic data, and to explore their potential immunopathological roles. - Source: PubMed
Publication date: 2025/07/15
Lv ChaoQi ChengangDai XiaokeZhang Mingman