F2RL3 Knockout Cell Lines

Gene: F2RL3

Official Full Name: F2R like thrombin or trypsin receptor 3provided by HGNC

Gene Summary: This gene encodes a member of the protease-activated receptor subfamily, part of the G-protein coupled receptor 1 family of proteins. The encoded receptor is proteolytically processed to reveal an extracellular N-terminal tethered ligand that binds to and activates the receptor. This receptor plays a role in blood coagulation, inflammation and response to pain. Hypomethylation at this gene may be associated with lung cancer in human patients. [provided by RefSeq, Sep 2016]

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Products Background Case study

Products

Catalog Number	Product Name	Species	Gene	Passage ratio	Mycoplasma testing	Price
KO00006	F2RL3 Knockout cell line （Huh-7）	Human	F2RL3	1:2~1:3	Negative	Online Inquiry
KO00972	F2RL3 Knockout cell line (Hep G2)	Human	F2RL3	1:2~1:4	Negative	Online Inquiry

Background

F2RL3 Gene Knockout Cell Lines are specifically engineered cellular models designed to facilitate the study of the F2RL3 gene, also known as the protease-activated receptor 3 (PAR3), which is implicated in various physiological and pathological processes. These knockout cell lines have been created through the targeted disruption of the F2RL3 gene using advanced genome-editing techniques, enabling researchers to understand its role in cell signaling pathways, inflammation, and immune response regulation.

The key function of F2RL3 Gene Knockout Cell Lines lies in their ability to provide insights into the mechanisms of F2RL3 deficiency. By studying these cell lines, scientists can observe alterations in cellular behavior, including changes in gene expression, metabolic activity, and overall cellular physiology. These knockout models allow for the elucidation of the biological consequences of F2RL3 knockouts, which can directly inform the understanding of disease mechanisms such as cardiovascular diseases, certain cancers, and immune disorders.

In the realm of research and clinical applications, these cell lines are invaluable for drug discovery and development. They provide a robust platform for testing therapeutic agents targeting the F2RL3 pathway and assessing their efficacy in relevant biological contexts. Moreover, by serving as a reference model for gene function studies, they enhance the depth of genetic research, potentially leading to breakthroughs in personalized medicine approaches.

Compared to alternative models, such as wild-type cell lines or transient knockdown systems, F2RL3 Gene Knockout Cell Lines offer stable gene disruption, ensuring reproducibility and consistency across experiments. This stability is crucial when investigating long-term effects of F2RL3 absence and evaluating therapeutic strategies.

Researchers and clinicians will find significant value in these cell lines as they streamline experimental workflows and deliver precise data about the F2RL3 gene's role in human health and disease. Our company possesses extensive expertise in genetic engineering and cell line development, ensuring high-quality, reliable products that empower scientific discovery and clinical innovation.

Case study

F2RL3 Gene Knockout Cell Lines for Pulmonary Hypertension Research

Research Focus

Investigate the function of F2RL3 (F2R like thrombin or trypsin receptor 3) in pulmonary hypertension (PH), specifically its role in endothelial dysfunction, interferon signaling regulation, and BMPR2 pathway modulation.

Background

1. Pulmonary Hypertension and Endothelial Dysfunction

PH is a severe vascular disease characterized by pulmonary arterial remodeling, driven by endothelial injury and inflammation. Mutations in BMPR2 (bone morphogenetic protein receptor 2) are a primary genetic cause, but inflammation acts as a "second hit" to trigger disease progression . The cGAS-STING signaling pathway, a key innate immune pathway, is activated in PH and associated with endothelial dysfunction .

2. Role of F2RL3 in PH

F2RL3 encodes protease-activated receptor-4 (PAR-4), which is upregulated in PH patients and rodent models. However, its mechanistic role in PH and interaction with STING-BMPR2 pathways remain unclear .

3. Gaps in Knowledge

How does F2RL3 contribute to PH pathogenesis?

What is the relationship between F2RL3, STING, and BMPR2 signaling?

Can F2RL3 knockout (KO) cell lines serve as a model to study PH therapeutic targets?

Solution

1. Generation of F2RL3 KO Cell Lines

Method: CRISPR-Cas9 genome editing was used to disrupt the F2RL3 gene in human pulmonary artery endothelial cells (PAECs). Guide RNAs targeted the F2RL3 coding sequence, and KO was confirmed by western blotting and qPCR .

Validation: F2RL3 KO PAECs showed reduced F2RL3 protein expression and altered endothelial function, including decreased proliferation and migration .

2. Functional Assays in F2RL3 KO Cells

Interferon Signaling: F2RL3 KO significantly reduced TNF-α-induced activation of the cGAS-STING pathway, as evidenced by decreased phosphorylation of IRF3 and TBK1, and reduced expression of interferon-stimulated genes (ISGs, e.g., IFIT1, CXCL10) .

BMPR2 Pathway: F2RL3 KO enhanced BMPR2 signaling, as shown by increased phosphorylation of Smad1/5/9 and upregulated BMPR2 protein levels .

Endothelial Dysfunction: F2RL3 KO cells exhibited reduced proliferation, migration, and endothelial activation marker ICAM-1 expression, mimicking the protective effects of STING inhibition .

3. Mechanistic Studies

STING-F2RL3 Interaction: Co-immunoprecipitation confirmed direct binding between STING and F2RL3 in PAECs. F2RL3 KO blocked STING-mediated repression of BMPR2 signaling .

Negative Feedback with BMPR2: BMP9 treatment repressed F2RL3 expression, while BMPR2 knockdown upregulated F2RL3, indicating a reciprocal regulatory loop .

Conclusion

1. Mechanistic Insights

F2RL3 acts as a downstream mediator of STING in PH, contributing to pathogenesis by:

Activating interferon signaling through STING-IRF3 axis .

Repressing BMPR2 signaling, which is critical for endothelial homeostasis .

Promoting endothelial cell proliferation and migration, exacerbating vascular remodeling .

2. Translational Significance

Disease Modeling: F2RL3 KO cell lines recapitulate key PH features, including interferon hyperactivity and BMPR2 dysfunction, providing a platform for studying disease mechanisms .

Therapeutic Targets: Inhibition of F2RL3 may represent a novel strategy to restore BMPR2 signaling and mitigate PH, complementing existing STING-targeted therapies .

3. Product Utility

F2RL3 KO cell lines offer unique value for:

Investigating the STING-F2RL3-BMPR2 axis in PH.

Screening compounds that modulate interferon signaling or BMPR2 activity.

Modeling endothelial dysfunction in preclinical PH research.

Please note that all services are for research use only. Not intended for any clinical use.

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