mProX™ Human CRHR1 Stable Cell Line

Product Information

Target Protein

CRHR1

Target Family

CRF Receptor Family

Target Protein Species

Mouse

Host Cell Type

bEnd3;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

CNS Research;Digestive and Renal Research

Related Diseases

Irritable Bowel Syndrome;Anxiety

Gene ID

Mouse: 12921

UniProt ID

Mouse: P35347

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

CRHR1, or Corticotropin-releasing hormone receptor 1, is a receptor that plays a pivotal role in the stress response system. In scientific research, CRHR1 has been extensively studied for its involvement in stress-related disorders, including depression and anxiety. Recent studies have shown that CRHR1 antagonists can be potential therapeutic agents for treating depression and anxiety disorders. These antagonists work by blocking the action of CRH, thereby reducing the stress response and alleviating symptoms of these disorders. Moreover, CRHR1 has also been linked to alcohol consumption behaviors, suggesting its potential role in alcohol use disorders. Understanding the molecular mechanisms and pathways involving CRHR1 can pave the way for novel therapeutic interventions for various stress-related conditions.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Linda (Verified Customer)

What is the significance of CRHR1 in the context of scientific research? Feb 21 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

CRHR1, also known as Corticotropin-releasing hormone receptor 1, plays a pivotal role in the stress response system. In scientific research, it has been identified as a key receptor involved in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for the body's response to stress. Dysregulation of this receptor can lead to various psychiatric and neurological disorders, making it a potential therapeutic target. Feb 21 2020

chat Cynthia (Verified Customer)

How does CRHR1 influence the body's response to stress? Aug 25 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

CRHR1 mediates the release of corticotropin-releasing hormone (CRH), which in turn stimulates the release of adrenocorticotropic hormone (ACTH) from the pituitary gland. This cascade eventually leads to the secretion of cortisol, a stress hormone, from the adrenal glands. Any alteration in the function of CRHR1 can disrupt this cascade, potentially leading to disorders related to stress response. Aug 25 2023

Published Data

Fig.1 CRHR1 knockdown inhibited H₂O₂-increased cerebral endothelial permeability in vitro.

Endothelial permeability in bEnd3 cells infected with lentivirus was assessed through the FITC-dextran transwell assay. After serum starvation of lentivirus-infected bEnd3 cells for 4 hours, they were exposed to H₂O₂ (2 mM) for 1 hour. Fluorescence intensity was standardized against shNC-infected cells treated with the vehicle. The data, represented as mean ± SEM, were derived from four groups. Significant differences were denoted as **P < 0.01, and ***P < 0.001; while #P < 0.05, ##P < 0.01, and ###P < 0.001 indicated other noteworthy observations.

Ref: Cao, Changchun, et al. "Activation of CRHR1 contributes to cerebral endothelial barrier impairment via cPLA2 phosphorylation in experimental ischemic stroke." Cellular Signalling 66 (2020): 109467.

Pubmed: 31715260

DOI: 10.1016/j.cellsig.2019.109467

Research Highlights

Kuznetsov A, et al. "Genetic Contributors to PTSD: the Role of SNVs, Gene Interactions and Haplotypes ." Psychiatria Danubina, 2023.
Post-traumatic stress disorder (PTSD) is a mental health condition characterized by trauma or stressors and has a significant impact on society. The authors conducted a review to identify genetic markers associated with PTSD, which could inform future prevention and treatment strategies. A search of the PubMed database yielded 547 articles, of which 20 met the inclusion criteria. Results showed significant correlations between PTSD and FKBP5 variants, as well as gene-gene interactions between DRD and OXTR-DRD. However, understanding of the polygenic and epigenetic mechanisms underlying PTSD remains limited and should be a focus of future research.
Pubmed: 37800217 DOI: No

Mei L, et al. "Identification of candidate genes and chemicals associated with osteoarthritis by ." Arthritis research & therapy, 2023.
Osteoarthritis (OA) is a prevalent degenerative joint disease affecting seniors, causing persistent discomfort and disability. Multiple risk factors contribute, such as aging, obesity, genetic predisposition, and environmental influences. A transcriptome-wide association study (TWAS) and chemical-related gene set enrichment analysis (CGSEA) were conducted to investigate the susceptibility genes and environmental elements. Using summary-level data from knee OA (KOA) and hip OA (HOA) genome-wide association studies, expression weights from the Genotype-Tissue Expression Project (Version 8) were integrated via the FUSION software for both single-tissue and cross-tissue TWAS. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) databases were utilized to analyze the biological function and pathways of TWAS genes, whilst the human cartilage mRNA expression profiles were used to validate them. In addition, CGSEA analysis was used to identify OA-associated chemicals by combining TWAS results with chemical-related gene sets. Results from both TWAS and CGSEA found 44 and 93 unique susceptibility genes, respectively, for KOA and HOA, across multiple chromosomes, with several showing significantly altered expression in mRNA profiles. These genes are involved in pathways such as TGF-beta signaling, MAPK signaling, hyaluronan metabolism, and chondrocyte differentiation. Furthermore, CGSEA identified 45 OA-associated chemicals, including quercetin, bisphenol A, and cadmium chloride. These findings offer insight into the relationship between genes, chemicals, and their impact on OA development and progression.
Pubmed: 37749624 DOI: 10.1186/s13075-023-03164-x