Ask about this productRelated genes to: RARB antibody
- Gene:
- RARB NIH gene
- Name:
- retinoic acid receptor beta
- Previous symbol:
- -
- Synonyms:
- HAP, NR1B2, RRB2
- Chromosome:
- 3p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-16
- Date modifiied:
- 2017-07-07
Related products to: RARB antibody
Related articles to: RARB antibody
- Although exercise is the most effective strategy for increasing the skeletal muscle mass, the underlying molecular mechanisms remain poorly understood. We previously demonstrated that β-carotene, a provitamin A compound, enhances muscle mass through a retinoic acid receptor γ (RARγ)-dependent pathway. However, the involvement of vitamin A in exercise-induced muscle hypertrophy remains unclear. In this study, we used a mouse model of functional overload to mimic resistance exercise and investigated the role of vitamin A in overload-induced muscle growth. Overload increased the expression of Rdh10, Dhrs9 and Aldh1a2, an enzyme required for active vitamin A synthesis in the skeletal muscle. In contrast, the expression of Aldh1a1, Dhrs3, and Rarb was decreased by the overload. Vitamin A deficiency significantly suppressed overload-induced muscle hypertrophy and protein synthesis. Moreover, local administration of an RAR antagonist to the skeletal muscle reduced overload-induced protein synthesis. These findings suggest that vitamin A contributes to skeletal muscle hypertrophy during muscle overload by promoting protein synthesis via RAR-mediated signaling. - Source: PubMed
Kitakaze TomoyaNakatsuji AinoHarada NaokiYamaji Ryoichi - Here we describe unrelated Japanese patients with distinct novel heterozygous retinoic acid receptor beta (RARB) gene variants underlying syndromic microphthalmia-12: case 1 with a frameshift variant, c.1205_1206del, had bilateral microphthalmia, corneal opacity, anterior segment dysgenesis, widespread multiorgan anomalies, hypotonia and cognitive impairment; case 2 with a missense variant, c.844G>T had Peters anomaly, extreme microphthalmia, spasticity, profound psychomotor delay and refractory epilepsy. These findings highlight the need for RARB testing. - Source: PubMed
Publication date: 2026/04/06
Koyanagi YoshitoMorikawa-Anzai HazukiYoshida TomoyoTominaga MakikoAbe YuichiKosaki RikaMatsubara KeikoFukami MakiNishina Sachiko - Clutch length is a key determinant of reproductive efficiency in geese and strongly positively correlates with egg production. We recorded daily egg production in 280 individually housed Zi geese, calculated clutch-related indices, and selected 12 geese to form long-clutch (LC) and short-clutch (SC) groups for ovarian transcriptomic, proteomic, and metabolomic analyses. The results showed that egg number, large clutch length, large clutch number, average clutch length, and average clutch number were significantly higher in LC than in SC groups (P < 0.0001). Transcriptomic analysis identified 885 differentially expressed genes enriched in oocyte development and ovarian steroidogenesis, with APOB, PLA2G4C, MMP2, MMP9, and NOBOX as key genes; proteomic analysis identified 437 differentially abundant proteins enriched in arachidonic acid metabolism and mitophagy, with CXCL12, RARB, and MAD2L1 as key proteins; and metabolomic analysis identified 35 differentially abundant metabolites enriched in glycolysis/gluconeogenesis, with lactic acid, guanidinoacetic acid, and 3-hydroxybutyrylcarnitine as key metabolites. Integration of multi-omics datasets highlighted a lactate-associated cross-omics signature supported by YWHAZ at the protein level and by the lactate transporter SLC16A3. Collectively, these findings deepen our understanding of the molecular basis underlying clutch-length variation in goose ovaries and highlight candidate genes, proteins, and metabolites for future functional validation. - Source: PubMed
Publication date: 2026/03/02
Wang HechuanLiu YunuoJiang KeYin JiaxinCong KexinMiao XinyiYang WeiranZhang YingLiu Shengjun - - Source: PubMed
Publication date: 2026/03/02
Skalski MarcinKowal-Wiśniewska EwelinaJaskiewicz-Rajewicz KatarzynaKiwerska KatarzynaBartochowska AnnaUstaszewski AdamGórecki TomaszMajchrzak-Celińska AleksandraWierzbicka MałgorzataJarmuż-Szymczak MałgorzataPaluszczak Jarosław - Genome-wide association studies have identified 1p36.23 as a schizophrenia risk locus. However, the functional variants and genes driving the association remain unknown. Here, we identified two functional variants (i.e., rs159961 and rs301792) at the 1p36.23 risk locus. Both variants reside introns of RERE and exhibit allele-specific enhancer activity. Risk alleles of rs159961 and rs301792 increase enhancer activity by altering REST and POLR2A binding, leading to RERE upregulation. Consistently, RERE was significantly elevated in brains of schizophrenia cases. Functionally, RERE-overexpression impaired neurogenesis, altered dendritic spine density and dendritic complexity, and altered genes related to dendrite development and glutamatergic synapses. Through interacting with RARB and RXRA at the Grin2a promoter, RERE regulates the well-known schizophrenia risk gene Grin2a (encodes an NMDAR subunit), and RERE-overexpression impairs excitatory synaptic transmission. Our study indicates that functional variants rs159961 and rs301792 confer schizophrenia risk by upregulating RERE, which affects neuronal development and synaptic function. - Source: PubMed
Publication date: 2026/01/24
Liu YixingWang JunyangYang HongLi YifanMu ChanggaiDang XinglunChen XinranLi DanyangLi MingnaLiu JieweiLi ShiwuYang JinfengChen XiZhang ChenFeng JinLuo Xiong-Jian