mProX™ Human HRH3 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types
S01YF-1122-KX531	Magic™ Dog HRH3 in Vitro [35S]GTPγS binding Assay	Dog	CHO-K1	[35S]GTPγS binding Assay
S01YF-1122-KX536	Magic™ Rat HRH3 in Vitro [35S]GTPγS binding Assay	Rat	CHO-K1	[35S]GTPγS binding Assay
S01YF-1122-KX537	Magic™ Rat HRH3 in Vitro Radioligand Binding Assay	Rat	CHO-K1	Radioligand Binding Assay

Product Information

Target Protein

HRH3

Target Family

Histamine Family

Target Protein Species

Human

Host Cell Type

H975;H460;A549;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

CNS Research

Related Diseases

Central Nervous System Disease;Kleine-Levin Hibernation Syndrome

Gene ID

Human: 11255

UniProt ID

Human: Q9Y5N1

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

Histamine receptor H3 (HRH3) has been associated with various diseases and conditions. Polymorphisms in the HRH3 gene have been linked to chronic heart failure in the Chinese Han population, suggesting its potential as a genetic marker for disease prediction and treatment. Additionally, the expression of HRH3 in brain endothelial cells has been studied, emphasizing its role in regulating brain capillary permeability.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Dorothy (Verified Customer)

How is the HRH3 gene expressed in brain endothelial cells? Apr 01 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

Brain vascular endothelial cells express histamine H1 and H2 receptors, which regulate brain capillary permeability. It has been found that H3 and H4 receptors are also expressed in these cells, suggesting they may play a role in permeability regulation. Apr 01 2022

chat Helen (Verified Customer)

Are there any pharmacogenetic studies related to the HRH3 gene and its therapeutic implications? Apr 09 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

Polymorphism of the HRH3 gene may be a potential genetic marker for predicting the therapeutic effect of the antipsychotic drug risperidone. Apr 09 2022

Published Data

Fig.1 Hrh3 protein knockdown regulated cellular motility and invasion.

Cell migration was assessed using a wound-healing assay, while cell invasion was quantified through the Transwell assay. Statistical significance denoted as *P < 0.05, **P < 0.01, ***P < 0.001 in comparison to the siNC group. Images captured at ×100 and ×200 magnification.

Ref: Zhao, Yan-yan, et al. "Inhibition of histamine receptor H3 suppresses the growth and metastasis of human non-small cell lung cancer cells via inhibiting PI3K/Akt/mTOR and MEK/ERK signaling pathways and blocking EMT." Acta Pharmacologica Sinica 42.8 (2021): 1288-1297.

Pubmed: 33159174

DOI: 10.1038/s41401-020-00548-6

Research Highlights

Tian LI, et al. "Targeting LncRNA LLNLR-299G3.1 with antisense oligonucleotide inhibits malignancy ." Oncology research, 2023.
Recent studies have demonstrated the crucial involvement of long non-coding RNAs (lncRNAs) in the progression of various cancers, including esophageal squamous cell carcinoma (ESCC). However, the specific mechanisms by which lncRNAs contribute to ESCC remain unclear, making it difficult to develop effective therapies. In this research, a novel ESCC-associated lncRNA, LLNLR-299G3.1, was identified through RNA-sequencing analysis. This lncRNA was found to be up-regulated in ESCC tissues and cells, and its silencing with antisense oligonucleotides (ASOs) inhibited ESCC cell proliferation and invasion. Further investigation revealed that LLNLR-299G3.1 interacts with cancer-associated RNA binding proteins and modulates the expression of cancer-related genes, such as OSM, TNFRSF4, HRH3, and SSTR3. ChIRP-seq analysis showed that these genes contain chromatin binding sites for LLNLR-299G3.1. Rescue experiments confirmed the importance of LLNLR-299G3.1's interaction with HRH3 and TNFRSF4 in promoting ESCC cell proliferation. To target LLNLR-299G3.1 in vivo, placental chondroitin sulfate A binding peptide-coated nanoparticles loaded with ASOs (pICSA-BP-ANPs) were developed and effectively suppressed ESCC tumor growth and improved animal survival. These findings suggest that LLNLR-299G3.1 promotes ESCC progression through gene-chromatin interactions and the use of pICSA-BP-ANPs may be a promising therapeutic approach for lncRNA-associated ESCC.
Pubmed: 37415734 DOI: 10.32604/or.2023.028791

Ji Q, et al. "Genetic and neural mechanisms of sleep disorders in children with autism spectrum ." Frontiers in psychiatry, 2023.
The prevalence of sleep disorders in children with autism spectrum disorder (ASD) is high and can negatively impact development and cause challenges for families and society. The complex pathological mechanism of sleep disorders in autism may involve gene mutations and neural abnormalities. This review examines literature on the genetic and neural mechanisms of sleep disorders in children with ASD. Eligible studies published between 2013 and 2023 were identified through searches of the databases PubMed and Scopus. The literature suggests that mutations in various genes, such as MECP2, VGAT, SLC6A1, HRH1, HRH2, HRH3, KCNQ3, PCDH10, AHI1, ARHGEF10, UBE3A, SLC6A3, PTCHD1, HTR2A, SLC6A4, MAOA, MAOB, TPH2, VMATs, SHANK3, CADPS2, ASMT, MTNR1A, and MTNR1B, can affect neural circuits associated with sleep-wake regulation and lead to sleep disorders in children with ASD. Understanding these mechanisms may help inform treatment strategies for children with ASD and sleep disorders.
Pubmed: 37200906 DOI: 10.3389/fpsyt.2023.1079683