huFCER1A Mouse
Product Name
huFCER1A Mouse
Product ID
C002090
Strain Name
C57BL/6NCya-Fcer1atm1(hFCER1A)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “huFCER1A Mouse (Catalog C002090) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
FCER1A
Gene Alias
FCE1A, FcERI, FCERIA
NCBI ID
Chromosome
Chr 1 (Human)
MGI ID
Datasheet
Strain Description
The α subunit of the high-affinity immunoglobulin E (IgE) receptor (FCER1A), also known as FcεRIα, is a member of the immunoglobulin Fc receptor family and serves as the ligand-binding subunit of the high-affinity IgE receptor (FcεRI), playing a central role in type I hypersensitivity reactions and immune regulation. This receptor α subunit specifically binds the Fc portion of IgE with extremely high affinity. Upon allergen-induced cross-linking of the IgE-FcεRI complex, it triggers downstream signaling cascades such as Lyn kinase activation and calcium influx, leading to degranulation of mast cells and basophils, and the release of histamine, leukotrienes, cytokines, and other mediators. This initiates the classical immediate-type allergic reaction, contributing to the development of allergic diseases as well as anti-parasitic immunity [1]. FCER1A is primarily expressed on the surface of effector cells such as mast cells and basophils, and can also be detected in certain dendritic cells, monocytes, and eosinophils, indicating its importance in immune surveillance and inflammation regulation [2].
Studies have shown that FCER1A gene polymorphisms significantly influence serum total IgE levels and are closely associated with the susceptibility and severity of allergic diseases such as allergic asthma, allergic rhinitis, and chronic urticaria [3-4]. Based on its critical role in allergic reactions and immune regulation, the IgE/FCER1A signaling pathway has become an important therapeutic target for IgE-mediated allergic diseases such as asthma.
huFCER1A mice are a humanized model constructed using gene editing technology. In this model, the sequences from the start codon to the stop codon of the endogenous mouse Fcer1a gene were replaced with the sequences from the start codon to the stop codon of the human FCER1A gene. huFCER1A mice can be used to study the pathogenesis of IgE-mediated allergic diseases, such as allergic asthma, allergic rhinitis, and chronic urticaria. They are also suitable for preclinical pharmacodynamic evaluation of drugs targeting the IgE/FCER1A signaling pathway.
Reference
Kinet JP. The high-affinity IgE receptor (FcεRI): from physiology to pathology. Annu Rev Immunol. 1999;17:931-972.
Potaczek DP, Kabesch M. Different FCER1A polymorphisms influence IgE levels in asthmatics and non-asthmatics. Pediatr Allergy Immunol. 2013;24(5):441-449.
Tang RY, et al. A Co-Expressed Natural Antisense RNA FCER1A-AS Controls IgE-Dependent Immunity by Promoting Expression of FcεRIα. Microbiol Spectr. 2023;11(3):e0073323.
Rojo-Tolosa S, et al. Influence of Genetics on the Response to Omalizumab in Patients with Severe Asthma. Int J Mol Sci. 2023;24(8):7029.
Strain Strategy
The sequences from the start codon to the stop codon of the endogenous mouse Fcer1a gene were replaced with the sequences from the start codon to the stop codon of the human FCER1A gene.
Figure 1. Gene editing strategy of huFCER1A mice.
Application Area
Screening, development, and preclinical evaluation of FCER1A-targeted drugs;
Research on the pathogenesis and treatment methods of allergic diseases, such as asthma, allergic rhinitis, and chronic urticaria;
Mechanistic Study of the IgE/FCER1A Signaling Pathway.
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