Ask about this productRelated genes to: RTN4 antibody
- Gene:
- RTN4 NIH gene
- Name:
- reticulon 4
- Previous symbol:
- -
- Synonyms:
- NSP-CL, KIAA0886, NOGO, ASY
- Chromosome:
- 2p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2015-08-25
Related products to: RTN4 antibody
Related articles to: RTN4 antibody
- To evaluate the therapeutic effects of NAP2, a novel NgR1 antagonist peptide, on Alzheimer's disease (AD) pathology and to determine whether inhibition of the Nogo-A/NgR1/ROCK signaling axis can ameliorate neurodegenerative alterations in APP/PS1 mice. - Source: PubMed
Zhang ZhengTan HuiminShi FangDai JiajiaDing WeilongLi JunliangWang YukeYang RuiXu XinkeChen ChengXiao FeiHuang Li-AnLiu XiaoyanLiao RuiYan Li - - Source: PubMed
Cao GuijunMeng XianqingHan XiaodongLi Jinhua - Symmetric cell division entails the equal distribution of cellular components to daughter cells. However, the mechanisms governing organelle segregation remain elusive. The endoplasmic reticulum (ER), comprising perinuclear sheets and peripheral tubules in interphase, serves as a central hub for sensing cellular states and coordinating other organelle dynamics. Here, we show that upon mitotic entry, the ER undergoes reverse redistribution: tubular ER accumulates around the centrosomes, while sheet-like ER relocates to the periphery. Mechanistically, the tubular ER protein Reticulon 4 (RTN4) is phosphorylated by cyclin-dependent kinase 1 (CDK1) during early mitosis. Phosphorylation promotes the interaction between RTN4 and Rab11, leading to the dynein-dependent enrichment of RTN4 around centrosomes and consequently driving the tubularization of the pericentrosomal ER. RTN4-mediated mitotic ER reorganization ensures symmetric distribution and inheritance of the ER, further contributing to the symmetric segregation of other organelles and mitotic fidelity. Thus, our study uncovers the mechanism of ER symmetry remodeling during early mitosis and its roles in organelle inheritance and mitotic progression. - Source: PubMed
Publication date: 2026/06/22
Xu XiangyuLiu YalinWang RongyiXu WenwenShi HaoHuang NingTeng JunlinMeng JinZheng PengliChen Jianguo - Nogo (RTN4) proteins and their receptors have emerged as candidate mediators of metabolic regulation and vascular pathology relevant to type 2 diabetes (T2D). The primary objective of this PRISMA-guided systematic review was to evaluate the clinical and cohort evidence for RTN4/RTN4R as potential biomarkers of T2D progression and vascular complications. A secondary objective was to synthesize preclinical mechanistic evidence on the effects of Nogo axis modulation on pathways relevant to the pathogenesis of T2D. We performed a PRISMA-guided systematic review. The protocol was not prospectively registered in PROSPERO. To ensure reproducibility, we provide complete search keywords, the screening log and the full-text exclusion table. PubMed/MEDLINE, EMBASE and Web of Science were searched for studies published 2000-2025; full search keywords are provided in the main text. The search strategy combined and free-text terms with Boolean operators. We included original preclinical and clinical studies, cohort/proteomic analyses, meta-analyses, and mechanistic papers reporting expression, function, signaling, or clinical associations of Nogo proteins/receptors in metabolic or vascular outcomes. Exclusion criteria: non-English articles, unclear methods, studies outside 2000-2025, and studies lacking primary data. Two reviewers independently screened records; conflicts were resolved by consensus. Study quality was appraised using established tools (SYRCLE for animal studies, Newcastle-Ottawa Scale for cohort/case-control studies). Preclinical evidence supports tissue-specific roles for RTN4 isoforms and receptors in the regulation of insulin secretion, proGCG → GLP-1 processing, ER homeostasis, and vascular permeability through the Src/PI3K/Akt and RhoA/ROCK axes. Cohort and proteomic analyses report associations between RTN4/RTN4R or serum NogoB and faster progression of T2D or vascular complications, but genetic assessment of causality (Mendelian randomization) has so far provided limited support in available data sets. Findings are heterogeneous with respect to directionality and tissue localization. RTN4 signaling exhibits tissue-specific mechanisms relevant to glucose regulation and vascular biology and warrants further translational study. However, heterogeneity across studies and limited genetic support for causality indicate that isoform-specific quantitative validation, longitudinal cohorts and integrated genetic-functional analyses are required before RTN4/RTN4R can be considered as clinical biomarkers. - Source: PubMed
Publication date: 2026/06/05
Bogdanović Jelena MBabić IvanaStanarčić Gajović JelenaLukač Sandra SinghMijač DraganaPopović DušanRanković IvanPopović LjiljanaRasulić IvaLalić Katarina - Alzheimer's disease (AD) is increasingly understood as a disorder driven not only by amyloid and tau pathology but also fundamentally shaped by underlying genetic mutations. By integrating multiple AD gene expression datasets with machine learning approaches-including random forest, XGBoost, LASSO, and SVM-we identified 172 differentially expressed genes, with TUBB2A, RTN4, and YWHAZ emerging as top mutation-associated hub genes. Critically, TUBB2A not only exhibited strong diagnostic potential (AUC = 0.822) but also harbored somatic mutations in our patient cohort, directly linking mutational events to disease manifestation. Unsupervised clustering revealed two distinct AD subtypes: one marked by widespread early gene overexpression and another (Cluster 2) dominated by endoplasmic reticulum stress-likely reflecting divergent mutational landscapes. Pseudotemporal trajectory analysis demonstrated a continuous progression from normal samples to Cluster 2, suggesting that a pivotal mutational event may initiate this transition and accelerate disease progression. These findings underscore the central role of somatic and germline mutations-particularly in TUBB2A-in AD pathogenesis. Our study strongly supports a paradigm shift toward mutation-centric biomarker development and advocates for SNP-based strategies to enable early diagnosis and personalized therapeutic interventions tailored to individual mutational profiles. - Source: PubMed
Publication date: 2026/05/12
Ma WanZhou FenfangCai HuayingFang Ling