Ask about this productRelated genes to: NUS1 antibody
- Gene:
- NUS1 NIH gene
- Name:
- NUS1 dehydrodolichyl diphosphate synthase subunit
- Previous symbol:
- C6orf68
- Synonyms:
- MGC7199, NgBR, TANGO14
- Chromosome:
- 6q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-08
- Date modifiied:
- 2019-01-22
Related products to: NUS1 antibody
Related articles to: NUS1 antibody
- Adiponectin signaling is essential for hepatic glucose homeostasis, yet the molecular basis of adiponectin receptor responsiveness remains incompletely understood. Here, we identify the Nogo-B receptor (NgBR; NUS1) as a regulator of hepatic adiponectin sensitivity. Across human, cynomolgus monkey, and mouse datasets, hepatic NgBR expression is consistently reduced in obesity-associated diabetes, indicating a conserved metabolic signature. Hepatocyte-specific NgBR deletion abolishes the metabolic effects of the adiponectin agonist AdipoRon, resulting in impaired AMPK activation, persistent gluconeogenesis, and ceramide accumulation. Mechanistically, NgBR loss suppresses KAT7 expression and reduces histone acetylation at AdipoR1 and AdipoR2 promoters, thereby limiting receptor expression. Adeno-associated virus (AAV)-mediated restoration of hepatic NgBR reinstates KAT7-dependent chromatin activation, adiponectin receptor expression, and glucose homeostasis. These findings support a hepatocellular mechanism in which NgBR maintains adiponectin receptor competence and suggest a potential therapeutic strategy for restoring adiponectin responsiveness in metabolic disease. - Source: PubMed
Publication date: 2026/05/22
Mohiuddin Mohammad SarifTirumalasetty Munichandra BabuHu WenquanBarua RashuWahiduzzaman MdChoubey MayankSchwartz Gary JMiao Qing Robert - Recently, an autoantibody signature considered to be predictive of multiple sclerosis (MS) has been reported in an article by Zamecnik et al. published in Nature Medicine, which is characterized by immunoglobulin G (IgG) responses to peptides sharing the amino acid motif P-(SA)-x-(SGA)-R-(SN)-(LRKH). These results are highly important, all the more so as the same motif is present also in two proteins expressed by Epstein-Barr virus (EBV), a pathogen that likely plays a key role in MS pathogenesis. However, clinically relevant autoantibody responses often target conformational epitopes, and peptides often differ from their corresponding proteins in terms of conformation. We were therefore interested in whether these findings can be reproduced at protein level and may thus play a role also in vivo. Here, we report findings from complementary experiments employing a microarray covering nearly 10,000 human full-length proteins and using serum and cerebrospinal fluid samples from patients with a histopathologically confirmed diagnosis of MS. Our data show that prominent IgG responses to full-length proteins bearing the P-(SA)-x-(SGA)-R-(SN)-(LRKH) motif can indeed be found in a substantial proportion of MS patients, although considerable inter-patient variability exists in both the type and number of individual responses. Notably, these IgG responses were more pronounced in patients with histopathologically defined pattern II MS (which is characterized by intralesional IgG and complement deposition) and pattern III MS than in patients with pattern I MS in our study. New motif-bearing candidate antigens identified in this study include RBMY2FP, CHMP2B, SRSF8 (SFRS2B), NUS1 (NgBR, Nogo-B receptor), and RTN2. Further studies investigating the diagnostic, pathophysiological, therapeutic, and prognostic implications of this antibody signature, as well as the potential role of cross-reactivity with EBV-suggested by the presence of the motif of interest in both EBV BRRF2 and EBV envelope glycoprotein M-are warranted and may significantly advance our understanding of MS. - Source: PubMed
Publication date: 2026/04/08
Jarius SRuprecht KMetz IKönig F BHaas JBrück WPaul FWildemann B - Epilepsy with myoclonic and atonic seizures (EMAtS), also known as Doose syndrome, accounts for 1%-2% of childhood epilepsies, and various genes have been implicated in causing this epilepsy syndrome. encodes for Nogo-B receptor (NgBR), which stabilizes the dehydrodolichyl-diphosphate synthase complex in the endoplasmic reticulum, promoting its enzymatic activity (cis-IPTase) and thereby regulating cholesterol biosynthesis. Pathogenic variants in have been associated with movement disorder and epilepsy; however, the spectrum of epilepsy and electroencephalogram (EEG) phenotype has not been well characterized. - Source: PubMed
Publication date: 2026/01/21
Ahmadi SaumelFulton NatalieMorrissey MichaelLandre RebekahTomko StuartUrano FumihikoGuerriero Réjean M - - Source: PubMed
Publication date: 2026/02/12
Munoz-Chesta DanielaMendez AlejandraHidalgo MariaRubilar CarlaKramer VaskoTroncoso-Schifferli Monica - Progressive myoclonic epilepsies (PME) are rare genetic disorders typically presenting with myoclonus, seizures, and cognitive decline. While several genes are associated with PME, the gene has recently emerged as a potential cause. We report the case of a 41-year-old woman who presented with tics, myoclonus, and language difficulties followed by gait instability, tremor, absence seizures, and psychotic symptoms including persistent hallucinations and delusional misidentification. - Source: PubMed
Publication date: 2025/12/18
Sau CristinaLópez-Rodríguez SergiFalip MercèEsteve-Garcia AnnaSala-Padró JacintAguilera CinthiaNavarro-Romero AlbaLasa-Aranzasti AmaiaRodríguez-Bel LauraHernández-Pérez Guillermo