| Protein Name | F2R like thrombin or trypsin receptor 3 |
| Gene Name | F2RL3 |
| Uniprot | Q96RI0 (Human); O88634 (Mouse) |
| Synonym | F2RL3; PAR4; proteinase-activated receptor 4; F2R like thrombin/trypsin receptor 3; PAR-4; coagulation factor II (thrombin) receptor-like 3; protease-activated receptor-4; thrombin receptor-like 3 |
| Background | PAR4, also referred to coagulation factor II receptor-like 3 (F2RL3) or thrombin receptor-like 3, is a type I receptor protein of 41 kDa that encoded by the chromosome 19p13.11. It has 385 amino acids and belongs to the protease-activated receptor (PAR) subfamily. Other members of PAR family include PAR1, 2 and 3, and among them, PAR1 and PAR3 can be activated by thrombin, PAR2 and PAR4 by several serine proteases. PAR4 is also a component of the G-protein-coupled receptor (GPCR) family. |
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| CAT# | Product Name | Expression System | Protein Length | Solubilizing Agents |
| S01YF-1023-KX381 | NativeExtract™ Human F2RL3 Membrane Protein (Full length, Super Nanodisc) | HEK293 cells | Full length | Native Nanodisc |
| MPX3374K | MemDX™ Membrane Protein Human F2RL3 Expressed in vitro E.coli expression system, Full Length of Mature Protein | E.coli cell-free | Full length | Detergent |
| MP0815J | MemDX™ Membrane Protein Human F2RL3 (F2R like thrombin or trypsin receptor 3) for Antibody Discovery | HEK293 cells | Full length | N/A |
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Regulatory Element Modification
Creative Biolabs offers regulatory element modification services. The targeted manipulation of regulatory elements presents a compelling strategy for influencing the transcriptional output of the F2RL3 gene. Specifically, approaches designed to augment the expression of non-mutated, functional F2RL3 alleles, or conversely, to diminish the activity of deleterious mutant alleles, may represent an effective therapeutic avenue. This strategic intervention bears a notable mechanistic resemblance to ongoing investigations into the etiology and treatment of Fragile X Syndrome. Therefore, analogous principles could perhaps be applied to precisely control F2RL3 abundance, offering a refined approach to addressing conditions associated with its aberrant expression.
Gene Replacement Therapy
Creative Biolabs offers gene replacement therapy development services. In scenarios where the primary etiology of a given pathology stems from a loss-of-function mutation within the F2RL3 gene, the introduction of exogenous, functional copies of this gene may serve as a viable therapeutic intervention. This strategy aims to directly compensate for the endogenous, defective allele. Such gene augmentation approaches have been rigorously investigated and, indeed, successfully applied in the context of various other inherited genetic disorders. Therefore, it is plausible that these established methodologies could be judiciously adapted for the specific treatment of conditions demonstrably linked to F2RL3-related deficiencies.
DNA Methylation Modification
Creative Biolabs offers DNA methylation modification services. The observed correlation between smoking-induced epigenetic DNA hypomethylation within the F2RL3 locus and an elevated predisposition to myocardial infarction suggests a potential therapeutic avenue. Consequently, interventions precisely designed to target and modify DNA methylation patterns at specific CpG sites within the F2RL3 gene could conceivably offer a mechanism to regulate its transcriptional activity. Such targeted epigenetic reprogramming might, therefore, represent a strategy to mitigate the associated disease risk.
Creative Biolabs offers comprehensive and innovative services to drive the development of F2RL3 cell therapy. Please for more services.
Regulation of EMT and Angiogenesis
Creative Biolabs offers regulation of EMT and angiogenesis development services. Evidence indicates that F2RL3 significantly potentiates several aggressive cellular phenotypes characteristic of gastric cancer (GC). Specifically, this protein has been demonstrably linked to an enhancement of cellular proliferation, increased metastatic potential, heightened invasiveness, and accelerated angiogenesis within GC cells. Furthermore, F2RL3 appears to facilitate the epithelial-mesenchymal transition (EMT) in these same cells. Consequently, a therapeutic strategy that concurrently targets this critical intracellular signaling cascade alongside F2RL3 modulation might represent a promising avenue for intervention in gastric adenocarcinoma.
Functional Regulation and Reporter Assays
Creative Biolabs offers unctional regulation and reporter assays services. To elucidate the intricate regulatory mechanisms governing F2RL3 gene expression, one might strategically employ reporter constructs. This methodology involves the subcloning of various genomic fragments derived from the F2RL3 locus into plasmids upstream of a luciferase reporter gene. Subsequent transfection of these constructs into appropriate cellular systems permits the quantitative assessment of transcriptional activity via luciferase luminescence. Such systematic analyses can yield crucial insights into the precise identity and functional characteristics of the cis-regulatory elements that orchestrate F2RL3 transcription.
Diagnostic and Biomarker Approaches
Creative Biolabs offers diagnostic and biomarker approaches development services. The utility of F2RL3 methylation as a biomarker in the context of various pathologies, particularly coronary heart disease (CHD), warrants comprehensive investigation. Prior research has, in fact, posited that blood-based F2RL3 methylation levels could serve as a valuable diagnostic or prognostic indicator for CHD. This potential is especially relevant in specific patient demographics, notably older individuals or those with a documented history of myocardial infarction. Further rigorous studies are, therefore, essential to fully validate and delineate the clinical applicability of this epigenetic marker.
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