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
- For chemical probe and drug discovery campaigns, the pairing of mass spectrometry-based chemoproteomics with photoaffinity labelling has emerged as a favoured approach for target discovery and mode of action assignment. However, photocrosslinked peptide-compound adducts raise analytic challenges for quantitative binding site discovery. Here, to address these challenges, we establish the Silyl Ether Enables Chemoproteomic Interaction and Target Engagement (SEE-CITE) method. SEE-CITE incorporates a fully functionalized chemically cleavable photocrosslinking handle that enables precise site-of-labelling identification and head-to-head comparisons of relative binding site engagement by chemically diverse compounds. To ensure high-confidence localization of labelled residues, we extended the MSFragger algorithm of the FragPipe computational platform to report localization scores customized for photoaffinity labelling and SEE-CITE data. When applied to scout fragments and analogues of select FDA-approved kinase inhibitors, SEE-CITE delineates known drug binding sites and uncovers small-molecule binding sites that affect the protein activity of RTN4 and COX5A. - Source: PubMed
Publication date: 2026/04/27
Ngo ChauTakechi ShoSivakumar AdityaVillanueva MirandaYu FengchaoBall Andréa BRubio JavierBiletch ElijahBurton Nikolas RBoatner Lisa MKim PhillipTurmon Alexandra CPerumal NitheshLiesa MarcDivakaruni Ajit SNesvizhskii Alexey IBackus Keriann M - Mitochondrial DNA replication occurs at contact sites between the endoplasmic reticulum (ER) and mitochondria (ERMCS). Beyond the known role of the tubular ER protein RTN4, the factors regulating this process are poorly defined. Here, we show that repressing the ER protein ERLIN2 in human fibroblasts depletes ER-mitochondrial contact sites and inhibits mitochondrial DNA replication, as does silencing RTN4 or the ER-mitochondrial tether GRP75. GRP75 or RTN4 scarcity also decreases the level of the mitochondrial calcium uniporter (MCU), whose inhibition blocks mitochondrial DNA synthesis. Because ERMCS depletion did not diminish mitochondrial calcium, and MCU complex can transport manganese, we tested whether manganese could bypass these defects. Manganese supplementation restored mitochondrial DNA replication in cells lacking ERMCS or with inhibited MCU, identifying manganese as a critical mediator. We then considered mitochondrial transcription as a potential manganese target, since it provides both transcripts for gene expression and primers for DNA replication. In vitro, manganese inhibits transcription re-start and stimulates RNA synthesis at the light-strand origin of replication. These findings support a model in which ER-mitochondrial contact sites, in conjunction with MCU, deliver manganese from the ER to mitochondria to promote DNA replication, potentially by modulating mitochondrial RNA polymerase activity. - Source: PubMed
Lopez de Arbina AmaiaZamudio-Ochoa AngelicaMuñoz-Oreja MikelPerez-Rodriguez DiegoMosqueira-Martín LauraLasalandra RebeccaVillar-Fernandez MarinaFernandez-Pelayo UxoaRodriguez-Gomez LauraLee SeungtaeGil-Bea FranciscoOsinalde NereaVallejo-Illaramendi AinaraTemiakov DmitrySpinazzola AntonellaHolt Ian J - Neuroplasticity dysregulation is implicated in the early pathophysiology of schizophrenia. Nogo-A, a myelin- and neuron-associated inhibitor of structural plasticity, has been less studied in first-episode schizophrenia (FES) than brain-derived neurotrophic factor (BDNF). This study examined short-term changes in serum Nogo-A and BDNF in drug-naïve patients with FES. - Source: PubMed
Publication date: 2026/04/02
Dudaklı Burcu BesimUzel Helin KanOcak Mahmut SafaEsen Öksüzoğlu MakbuleLevent Çıraklı ZeynepKaramustafalıoğlu Nesrin - 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