更新于：2024-11-01

GHB receptor

更新于：2024-11-01

基本信息

别名

D15Ertd747e、FLJ11856、G protein-coupled receptor 172A

+ [14]

简介

(Microbial infection) In case of infection by retroviruses, acts as a cell receptor to retroviral envelopes similar to the porcine endogenous retrovirus (PERV-A). Plasma membrane transporter mediating the uptake by cells of the water soluble vitamin B2/riboflavin that plays a key role in biochemical oxidation-reduction reactions of the carbohydrate, lipid, and amino acid metabolism (PubMed:20463145, PubMed:22864630, PubMed:23243084, PubMed:24253200, PubMed:27702554). Humans are unable to synthesize vitamin B2/riboflavin and must obtain it via intestinal absorption (PubMed:20463145). May also act as a receptor for 4-hydroxybutyrate (Probable).

关联

项与 GHB receptor 相关的药物

UMB86

靶点

GABA transaminase x GHB receptor

作用机制

GABA transaminase agonists [+1]

在研机构

The University of Texas System

原研机构

The University of Texas System

在研适应症

发作性睡病

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

UMB-73

靶点

GHB receptor

作用机制

GHB receptor agonists

在研机构

The University of Texas System

原研机构

The University of Texas System

在研适应症

发作性睡病

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

NCS-382

靶点

GHB receptor

作用机制

GHB receptor拮抗剂

在研机构

University of Copenhagen

原研机构

University of Copenhagen

在研适应症

缺血性卒中 [+1]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 GHB receptor 相关的临床结果

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100 项与 GHB receptor 相关的转化医学

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0 项与 GHB receptor 相关的专利（医药）

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166

项与 GHB receptor 相关的文献（医药）

2024-09-01·Journal of Hazardous Materials

Fluoride induces immunotoxicity by regulating riboflavin transport and metabolism partly through IL-17A in the spleen

Article

作者: Cui, Yukun ; Zhang, Jianhai ; Tan, Yanjia ; Yang, Jie ; Wang, Jundong ; Yong, Yufei ; Lang, Yilin ; Li, Xiang ; Liang, Chen ; Cai, Miaomiao ; Zhuang, Cuicui ; Qiao, Yurou ; Zhang, Xinying ; Ren, Xuting

The impairment of the immune system by fluoride is a public health concern worldwide, yet the underlying mechanism is unclear. Both riboflavin and IL-17A are closely related to immune function and regulate the testicular toxicity of fluoride. However, whether riboflavin or IL-17A is involved in fluoride-induced immunotoxicity is unknown. Here, we first established a male ICR mouse model by treating mice with sodium fluoride (NaF) (100 mg/L) via the drinking water for 91 days. The results showed that fluoride increased the expression of the proinflammatory factors IL-1β and IL-17A, which led to splenic inflammation and morphological injury. Moreover, the expression levels of the riboflavin transporters SLC52A2 and SLC52A3; the transformation-related enzymes RFK and FLAD1; and the key mitochondrial functional determinants SDH, COX, and ATP in the spleen were measured via real-time PCR, Western blotting, and ELISA. The results revealed that fluoride disrupted riboflavin transport, transformation, metabolism, and mitochondrial function. Furthermore, wild-type (WT) and IL-17A knockout (IL-17A^-/-) C57BL/6 J male mice of the same age were treated with NaF (24 mg/kg·bw, equivalent to 100 mg/L) and/or riboflavin sodium phosphate (5 mg/kg·bw) via gavage for 91 days. Similar parameters were evaluated as above. The results confirmed that fluoride increased riboflavin metabolism through RFK but not through FLAD1. Fluoride also affected mitochondrial function and activated neutrophils (marked with Ly6g) and macrophages (marked with CD68) in the spleen. Interestingly, IL-17A partly mediated fluoride-induced riboflavin metabolism disorder and immunotoxicity in the spleen. This work not only reveals a novel toxic mechanism for fluoride but also provides new clues for exploring the physiological function of riboflavin and for diagnosing and treating the toxic effects of fluoride in the environment.

2024-08-09·ACS Pharmacology & Translational Science

MicroPET Imaging of Riboflavin Transporter 3 Expression in Myocardial Infarction/Reperfusion Rat Models with Radiofluorinated Riboflavin

Article

作者: Zhang, Deliang ; Shi, Changrong ; Zeng, Xinying ; Yang, Hongzhang ; Li, Jindian ; Zhang, Xianzhong ; Chen, Yingxi ; Yin, Bin ; Guo, Zhide ; Hong, Xingfang

Riboflavin transporter 3 (RFVT3) represents a potential cardioprotective biotarget in energetic metabolism reprogramming after myocardial infarction/reperfusion (MI/R). This study investigated the feasibility of noninvasive real-time quantification of RFVT3 expression after MI/R with an radiolabeled probe ¹⁸F-RFTA in a preclinical rat model of MI/R. The tracer ¹⁸F-RFTA was radio-synthesized manually and characterized on the subjects of radiolabeling yield, radiochemical purity, and stability in vivo. MI/R and sham-operated rat models were confirmed by cardiac magnetic resonance imaging (cMRI) and single-photon-emission computed tomography (SPECT) myocardial perfusion imaging (MPI) with technetium-99m sestamibi (^99mTc-MIBI). Positron emission tomography (PET) imaging of MI/R and sham-operated rat models were conducted with ¹⁸F-RFTA. Ex vivo autoradiography and RFVT3 immunohistochemical (IHC) staining were conducted to verify the RFVT3 expression in infarcted and normal myocardium. ¹⁸F-RFTA injection was prepared with high radiochemical purity (>95%) and kept stable in vitro and in vivo. ¹⁸F-RFTA PET revealed significant uptake in the infarcted myocardium at 8 h after reperfusion, as confirmed by lower ^99mTc-MIBI perfusion and decreased intensity of cMRI. Conversely, there were only the tiniest uptakes in the normal myocardium and blocked infarcted myocardium, which was further corroborated by ex vivo autoradiography. The RFVT3 expression was further confirmed by IHC staining in the infarcted and normal myocardium. We first demonstrate the feasibility of imaging RFVT3 in infarcted myocardium. ¹⁸F-RFTA is an encouraging PET probe for imaging cardioprotective biotarget RFVT3 in mitochondrial energetic metabolism reprogramming after myocardial infarction. Noninvasive imaging of cardioprotective biotarget RFVT3 has potential value in the diagnosis and therapy of patients with MI.

2024-08-01·Acta Neurologica Belgica

Atypical presentations in an RTD patient and report of novel SLC52A3 and SLC52A2 mutations

Article

作者: Tonekaboni, Seyed Hassan ; Boostani, Reza ; Akhondian, Javad ; Alavi, Afagh ; Mirzadeh, Hanieh S ; Shamshiri, Hosein ; Elahi, Elahe ; Sabeghi, Donya ; InanlooRahatloo, Kolsoum ; Nafissi, Shahriar ; Ebrahimi, Masoomah ; Taghavi, Tarannomsadat ; Khani, Marzieh ; Salehi, Najmeh

INTRODUCTIONRiboflavin Transporter Deficiency (RTD) is a rare neurological disorder characterized by pontobulbar palsy, hearing loss, and motor cranial nerve involvement. SLC52A3 and SLC52A2 mutations are causes of RTD. SLC52A2 mutations are usually found in childhood onset cases. Fifteen Iranian RTD diagnosed patients without SLC52A2 mutations have been previously described. We aimed to identify causative mutations in two childhood cases.METHODSWe recruited patients with diagnosis of BVVL. Comprehensive clinical evaluations were performed on the patients. SLC52A3 and SLC52A2 genes were PCR-amplified and Sanger sequenced. Candidate disease causing variations were screened for segregation with disease status in the respective families and control individuals.RESULTSA novel homozygous SLC52A3 mutation (p.Met1Val) and a heterozygous SLC52A2 mutation (p.Ala288Val) were both observed in one proband with typical RTD presentations. The aggregate of presentations in the early stages of disease in the second patient that included weakness in the lower extremities, absence of bulbar or hearing defects, prominent sensory polyneuropathy as evidenced in electrodiagnostic studies, and absence of sensory symptoms including sensory ataxia did not prompt immediate RTD diagnosis. Dysarthria and decreased hearing manifested later in the disease course. A novel homozygous SLC52A2 (p.Val314Met) mutation was identified.CONCLUSIONA literature search found recent reports of other atypical RTD presentations. These include MRI findings, speech understanding difficulties accompanied by normal hearing, anemia, and left ventricular non-compaction. Knowledge of unusual presentations lessens the chance of misdiagnosis or delayed RTD diagnosis which, in light of favorable effects of riboflavin supplementation, is of immense importance.