Ask about this productRelated genes to: RTN4R antibody
- Gene:
- RTN4R NIH gene
- Name:
- reticulon 4 receptor
- Previous symbol:
- -
- Synonyms:
- NOGOR
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-30
- Date modifiied:
- 2019-02-26
Related products to: RTN4R antibody
Related articles to: RTN4R antibody
- 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 - Spinal cord injury (SCI) leads to severe and often permanent neurological deficits. The inhibitory Nogo/NgR signaling pathway constitutes a major barrier to axonal regeneration. Transplantation of bone marrow mesenchymal stem cells (BMSCs) and modulation of microRNAs, such as miR-let-7b, represent promising therapeutic strategies for neural repair. - Source: PubMed
Yang BeirenYu Aihua - This study systematically investigated the effects and molecular mechanisms of Baishaoluoshi Decoction (BD) on synaptic plasticity in rats with post-stroke spasticity (PSS). - Source: PubMed
Sun XiongxingZeng ShanshanLin ShigaoWu LingyingTang XukunZhu JiajianZhang YuhuiLi LuChen ZimingDeng XinyuWu DahuaXie Le - Younger-onset type 2 diabetes (T2D) (onset <40 years) represents a growing global health challenge, characterized by heterogenous pathophysiology and accelerated complications. Current one-size-fits-all treatment approaches may be inadequate for this population. To address this heterogeneity, we performed clinical variable-based clustering using BMI, onset age, HbA1c, and HOMA2 indices in 717 participants across discovery and validation cohorts. Three distinct subgroups were identified: mild obesity-related diabetes (MOD), severe insulin-deficient diabetes (SIDD), and severe insulin-resistant diabetes with insulin insufficiency (SIRD-II). Over median follow-up of 2.8 years, SIRD-II demonstrated 11-fold increased risk of progressive chronic kidney disease, while both SIDD and SIRD-II showed threefold increased risk for progressive albuminuria compared with MOD. SIRD-II also demonstrated 3.5-fold and 2.3-fold higher 10-year cardiovascular risk compared with SIDD and MOD respectively. Metabolomic analysis revealed distinct signatures: SIDD exhibited lower levels of lipids, amino acids, and inflammatory markers, while SIRD-II demonstrated elevated glucose, lipids, and branched-chain amino acids, suggesting glucolipotoxicity. Proteomics analysis validated previously reported biomarkers (IGFBP1, RTN4R, PLXNB2) and identified additional molecules (CDHR2, ERBB4, DPP6) that may shed light on disease mechanisms. In conclusion, younger-onset T2D exhibits distinct subgroups with differential pathobiology, molecular signatures, and clinical outcomes, suggesting the need for personalised precision diabetes care. - Source: PubMed
Tan Clara Si HuaKee Kai XiangZheng HuiliWong Kay Wye SabrinaChan Wan Ting LovynnSong YuzhenAng KevenSubramaniam TavintharanSum Chee FangLim Su Chi - BAI1, BAI2, and BAI3 (for 'Brain-specific Angiogenesis Inhibitor-1, -2, and -3') are adhesion-GPCRs implicated in neuronal development. The precise roles of individual BAIs remain unclear. BAIs interact with two sets of ligands, secreted C1ql proteins and membrane-bound RTN4R proteins (a.k.a. NoGo receptors), but which of these ligands regulate specific functions of BAIs is incompletely understood. To address these key questions, we here systematically examine the functions of the three BAIs in neuronal development using hippocampal neuron-glia cultures, genetic knockouts, and rescue experiments. In a direct comparison, we demonstrate that deletions of BAI1 or BAI3, but not of BAI2, increase axonal and dendritic arborizations but decrease excitatory synapse formation, while inhibitory synapse formation remains unaffected. Since biochemical and cellular assays reveal that only BAI3 binds to both RTN4Rs and C1qls, we analyzed the role of these two ligands in controlling BAI3 functions using rescue experiments. We find that RTN4R-binding to BAI3 is essential for restricting axonal and dendritic arborizations and for enabling excitatory synapse formation, whereas C1ql-binding to BAI3 is only required for synapse organization as monitored in hippocampal neuron-glia cultures. Thus, BAI1 and BAI3 perform diverse functions that shape multiple facets of neuronal development and that require their interaction with RTN4Rs. - Source: PubMed
Publication date: 2025/12/23
Wang JieWang JinzhaoMiao YiLi YangZhu ShaoyuanZhang YuYousif AhmedHuang MinWernig MariusSüdhof Thomas C