NOGO, affinity purified antibody, goat, 100 ug.
- Known as:
- NOGO, antigenic enriched (anti-), caprine, 100 ug.
- Catalog number:
- GT15154-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- NOGO affinity purified antibody goat 100 .
Related genes to: NOGO, affinity purified antibody, goat, 100 ug.
- 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
- 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: NOGO, affinity purified antibody, goat, 100 ug.
Related articles to: NOGO, affinity purified antibody, goat, 100 ug.
- 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 - 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 - 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 - 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 - Gene-based therapeutic strategies to lower ataxin-2 levels are emerging for the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and spinocerebellar ataxia type 2 (SCA2). Additional strategies to lower levels of ataxin-2 could be beneficial. Here, we perform a genome-wide arrayed small interfering RNA (siRNA) screen in human cells and identify RTN4R, the gene encoding the RTN4/NoGo-Receptor, as a potent modifier of ataxin-2 levels. RTN4R knockdown, or treatment with a peptide inhibitor, is sufficient to lower ataxin-2 protein levels in mouse and human neurons in vitro, and Rtn4r knockout mice have reduced ataxin-2 levels in vivo. We provide evidence that ataxin-2 shares a role with the RTN4/NoGo-Receptor in limiting axonal regeneration. Reduction of either protein increases axonal regrowth following axotomy. These data define the RTN4/NoGo-Receptor as a novel therapeutic target for ALS and SCA2 and implicate the targeting of ataxin-2 as a potential treatment following nerve injury. - Source: PubMed
Rodriguez Caitlin MBechek Sophia CJones Graham LNakayama LisaAkiyama TetsuyaKim GaramSolow-Cordero David EStrittmatter Stephen MGitler Aaron D