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
- Spinal cystic echinococcosis (CE) is a rare but serious zoonotic disease associated with significant morbidity, disability, and mortality in endemic regions. It has the potential to cause disability or death in more than half of those affected. Due to its complex pathological features, conventional drugs and surgical interventions are often ineffective, highlighting the pressing requirement for identifying novel therapeutic targets. This study aimed to clarify the function of Nrf2, which is highly expressed, in the neovascularization linked to cystic echinococcosis of the spinal cord and to investigate its potentially relevant molecular mechanisms. Establishing a co-culture system between protoscoleces (PSCs) and human umbilical vein endothelial cells (HUVECs) with high expression of Nrf2 significantly enhanced the proliferation, migration, and angiogenesis of HUVECs. Additionally, it exhibited significant anti-angiogenic effects in a cystic model of the spinal cord in Nrf2 knockout mice. Transcriptome sequencing revealed a strong correlation between RTN4 and Nrf2, and the upregulation and inhibition of RTN4 via lentivirus confirmed its impact on angiogenesis. The results indicated that RTN4 negatively correlated with Nrf2, inhibiting lumen formation in HUVECs when influenced by PSCs. Furthermore, RTN4 was found to be negatively regulated by Nrf2. In conclusion, Nrf2 might promote angiogenesis by inhibiting RTN4, positioning it as a potential therapeutic target for spinal cystic echinococcosis treatment. - Source: PubMed
Publication date: 2026/04/06
Huang YipingMa YiboWang SiboLiu YaqingSun HaohaoXiong KangjunRen QianShi Chenhui - There is still a lack of enough evidence about Nogo-B levels and vascular complications in patients with type 2 diabetes. Our first aim was to assess the levels of Nogo-B in type 2 diabetes mellitus (T2DM) patients with or without vascular complications (VC). Our second aim was to determine the mechanism by which Nogo-B may protect vasculature using a hyperglycemic HUVEC model. - Source: PubMed
Irakoze LaurentMa LinqiangGu YuanfengChen XiangjunZeng FanlingLuo RongLai YulianLi XunChen ShangbinBanderembako PaulNkengurutse LilianeLei XunXiao XiaoqiuCheng Qingfeng - Identify mitochondrial autophagy genes associated with Alzheimer's disease (AD) and elucidate its underlying pathogenesis and explore potential therapeutic targets. Alzheimer's disease related gene expression data were obtained from the Gene Expression Omnibus database. Mitochondrial autophagy-related genes with a relevance score > 1 were screened based on the GeneCards database. We identified differentially expressed genes using R, followed by functional enrichment and immune cell infiltration analyses. A protein-protein interaction network was constructed based on the STRING database, and key genes were identified by Cytoscape software. A diagnostic model for Alzheimer's disease was subsequently developed based on these key genes. Nine key genes were identified for Alzheimer's disease. Gene Ontology enrichment analysis revealed that the differentially expressed genes (DEGs) were primarily involved in mitochondrial function and nucleotide metabolism. Immune infiltration analysis showed negative correlations between YWHAG and VPS35 expression and M1 macrophage abundance, while RTN4 expression positively correlated with follicular helper T cell abundance. Using logistic regression analysis, a diagnostic model for AD was constructed based on three of the key genes. The model was validated by independent external samples, where area under the curve (AUC) demonstrated its robust and excellent diagnostic performance. The nine key genes identified in this study provide new insights and potential therapeutic targets for elucidating how mitochondrial autophagy influences Alzheimer's disease. The established diagnostic model provides a theoretical basis for personalized diagnosis and treatment of Alzheimer's disease. - Source: PubMed
Gao ZheWang YunRen YanfengLyu Juncheng - Receptor Expression-Enhancing Protein 5 (REEP5) is a cardiac-enriched, membrane-shaping protein localized to the sarco(endo)plasmic reticulum (SR/ER), where it supports membrane network architecture and cardiomyocyte function. While REEP5 has been implicated in calcium handling and contractility, its role in regulating inter-organelle communication and mitochondrial homeostasis remains less well-understood. In this study, we used recombinant adeno-associated virus serotype 9-mediated shRNA knockdown of Reep5 in mouse hearts, combined with subcellular fractionation and data-independent acquisition mass spectrometry, to define proteomic remodeling across microsomal (SR/ER), mitochondrial, and cytosolic compartments. Loss of REEP5 altered the composition of SR/ER membrane-shaping proteins, including upregulation of RTN4, ATL3, and CKAP4, suggesting a partial compensatory response. Microsomal, mitochondrial and cytosolic proteomes exhibited broad reorganization, with enrichment of proteins involved in redox adaptation and proteostasis, alongside depletion of mitochondrial import machinery and antioxidant enzymes. Imaging of isolated cardiomyocytes confirmed fragmented mitochondrial networks and increased reactive oxygen species, consistent with proteomic signatures of disrupted mitochondrial dynamics and oxidative stress. Gene ontology enrichment across all fractions highlighted widespread dysregulation in organelle-specific processes, including translation, protein localization, and metabolic remodeling. Notably, several altered pathways converged on mitochondria-associated membranes, suggesting that REEP5 may support SR/ER-mitochondria tethering and functional crosstalk. These findings position REEP5 as a key regulator of organelle homeostasis in the heart and underscore how its loss disrupts mitochondrial integrity and inter-organelle communication across cellular compartments. - Source: PubMed
Publication date: 2026/02/09
Di Paola MichelleReitz Cristine JKuzmanov UrosJia KateleenGramolini Anthony O - The pathophysiology of post-traumatic stress disorder (PTSD) shows notable associations with compromised hippocampal neurophysiology. Notwithstanding ongoing debates, PTBP1 knockdown (KD) demonstrates the capacity to drive glia-to-neuron reprogramming, potentially offering therapeutic benefits for some neurodegenerative pathologies. However, PTBP1 KD can upregulate the expression of Nogo-A by alternative splicing, triggering the inhibition of nerve regeneration. Currently, the role of PTBP1 in PTSD remains unknown. Here we sought to elucidate the neurorestorative effects of modulating the PTBP1/Nogo-A/NgR axis in a mouse model of PTSD established through the single prolonged stress paradigm, and the mechanisms were further investigated through a series of experiments including pathological and molecular detection. The results indicated that PTBP1 KD ameliorates PTSD-like behaviors in mice by balancing Bcl-2/Bax expression and suppressing Caspase-3 splicing activation to inhibit hippocampal neuronal apoptosis, enhancing synaptic plasticity through upregulating PSD95 and SYN1, increasing dendritic spine density and stabilizing axonal architecture via elevated NF200 expression. However, compared with single prolonged stress alone, PTBP1 KD potentiates the activation of Nogo-A/NgR pathway, adversely impacting both dendritic morphology and axonal elongation. Therefore, we proposed a combined KD of PTBP1 and NgR to counteract the adverse effects mediated by Nogo-A signal activation, effectively promoting dendritic growth and axonal extension in hippocampal neurons of PTSD mice. Our findings underscore the potential and limitations of PTBP1 as a therapeutic target and propose a novel method for PTSD treatment through combined target intervention of PTBP1 and NgR. This study provides a theoretical foundation for multitarget intervention strategies in the treatment of PTSD and related disorders. - Source: PubMed
Publication date: 2026/01/21
Liu Bing-YaoChen Xing-DongLiu Hui-LinWang Si-WeiSong Qian-ZhongCheng HuiLi SenWang Hai-YanLu Xiu-MinWang Yong-Tang