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Last update 23 Jan 2025

GHB receptor

Last update 23 Jan 2025

Basic Info

Synonyms

D15Ertd747e, FLJ11856, G protein-coupled receptor 172A

+ [14]

Introduction

(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).

Drugs associated with GHB receptor

UMB86

Target

GABA transaminase x GHB receptor

Mechanism

GABA transaminase agonists [+1]

Active Org.

The University of Texas System

Originator Org.

The University of Texas System

Active Indication

Narcolepsy

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

UMB-73

Target

GHB receptor

Mechanism

GHB receptor agonists

Active Org.

The University of Texas System

Originator Org.

The University of Texas System

Active Indication

Narcolepsy

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NCS-382

Target

GHB receptor

Mechanism

GHB receptor antagonists

Active Org.

University of Copenhagen

Originator Org.

University of Copenhagen

Active Indication

Ischemic stroke [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GHB receptor

100 Translational Medicine associated with GHB receptor

0 Patents (Medical) associated with GHB receptor

171

Literatures (Medical) associated with GHB receptor

10 Dec 2024·Neurology

Stable Visual and Neurologic Status With Continued Riboflavin Therapy

Article

Author: Shinawi, Marwan S. ; Culican, Susan M. ; Zaidman, Craig M. ; O'Brien, Marisa A.

Riboflavin transporter deficiency (RTD), previously referred to as Brown-Vialetto-Van Laere syndrome, is caused by pathogenic variants in the SLC52A1, SLC52A2, or SLC52A3 genes, resulting in RTD types 1, 2, and 3, respectively. Researchers estimate an occurrence of approximately 1 in 1,000,000. There is only one case of type 1 described in medical literature. Type 2 is characterized by muscle weakness in the arms and neck, vision loss, hearing impairment, and sensory ataxia. In type 3, vocal cord paralysis is more common and muscle weakness is more generalized. In 2018, we described a case of a 6-year-old girl with RTD type 2 who made remarkable visual recovery after initiation of treatment with oral riboflavin and coenzyme Q10 supplementation. The patient's younger brother began the same treatment regimen after genetic testing confirmed that he carried the same genetic variant. In this report, we update the visual and neurologic status in these siblings 5 years after our initial report and 7.5 years after initiation of riboflavin treatment.

01 Dec 2024·Clinical Pharmacology & Therapeutics

Rare Diseases Linked to Mutations in Vitamin Transporters Expressed in the Human Blood–Brain Barrier

Review

Author: Giacomini, Kathleen M. ; Yee, Sook Wah ; Wang, Joanne

Recent advances have significantly enhanced our understanding of the role of membrane transporters in drug disposition, particularly focusing on their influence on pharmacokinetics, and consequently, pharmacodynamics. The relevance of these transporters in clinical pharmacology is well acknowledged. Recent research has also underscored the critical role of membrane transporters as targets in human diseases, including their involvement in rare genetic disorders. This review focuses on transporters for water‐soluble B vitamins, such as thiamine, riboflavin, and biotin, essential cofactors for metabolic enzymes. Mutations in transporters, such as SLC19A3 (thiamine), SLC52A2, and SLC52A3 (riboflavin), and SLC5A6 (multiple B vitamins including pantothenic acid and biotin) are linked to severe neurological disorders due to their role in the blood–brain barrier, which is crucial for brain vitamin supply. Current treatments, mainly involving vitamin supplementation, often result in variable response. This review also provides a short perspective on the role of the transporters in the blood‐cerebrospinal fluid barrier and highlights the potential development of pharmacologic treatments for rare disorders associated with mutations in these transporters.

01 Sep 2024·Journal of Hazardous Materials

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

Article

Author: 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.

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GHB receptor

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