huRAGE(AGER)(BALB/c) Mouse
Product Name
huRAGE(AGER)(BALB/c) Mouse
Product ID
C002010
Strain Name
BALB/cAnCya-Agertm1(hAGER)/Cya
Backgroud
BALB/cAnCya
Status
When using this mouse strain in a publication, please cite “huRAGE(AGER)(BALB/c) Mouse (Catalog C002010) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
AGER
Gene Alias
RAGE, sRAGE, SCARJ1
NCBI ID
Chromosome
Chr 6 (Human)
MGI ID
Datasheet
Strain Description
AGER (advanced glycosylation end-product specific receptor, RAGE), a member of the immunoglobulin superfamily, acts as a multi-ligand receptor. In addition to binding to advanced glycation end-products (AGEs), it interacts with damage-associated molecular patterns (DAMPs), such as S100 proteins and HMGB1, participating in homeostasis maintenance, inflammatory responses, cell migration, and various pathological processes [1]. This receptor plays a critical role in the pathogenesis and progression of various diseases, including diabetic complications, atherosclerosis, neurodegenerative diseases, sepsis, pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), and tumors [2-4]. Studies have shown that polymorphisms in the human AGER gene are associated with the susceptibility to and severity of multiple inflammatory and metabolic diseases, and abnormally activated RAGE signaling can amplify inflammatory cascades and promote tissue damage [5].
The huRAGE(AGER)(BALB/c) mouse model is a humanized model constructed through gene-editing technology, in which the endogenous mouse Ager gene region spanning from the 5' UTR to the 3' UTR was replaced in situ with the corresponding human AGER gene sequence, including the G allele of the common p.G82S SNP. This model is established on the BALB/cAnCya genetic background and is suitable for studying the mechanisms underlying the human RAGE-AGEs axis in vascular inflammation, atherosclerotic plaque formation, and cardiovascular disease progression; investigating the role of human RAGE-mediated Aβ transport and neuroinflammation in the pathogenesis of Alzheimer's disease (AD) and related intervention strategies; evaluating the alleviating effects of human RAGE signaling inhibition on systemic inflammatory responses and multi-organ damage induced by damage-associated molecular patterns (DAMPs) such as HMGB1; studying the mechanisms by which human RAGE promotes epithelial cell activation and fibrosis in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD); as well as evaluating the pharmacological efficacy and safety of human RAGE-targeting therapeutics.
Reference
Dobrucki IT, Miskalis A, Nelappana M, Applegate C, Wozniak M, Czerwinski A, Kalinowski L, Dobrucki LW. Receptor for advanced glycation end-products: Biological significance and imaging applications. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2024 Jan-Feb;16(1):e1935.
Vitorakis N, Piperi C. Pivotal role of AGE-RAGE axis in brain aging with current interventions. Ageing Res Rev. 2024 Sep;100:102429.
Yang K, Fan M, Wang X, Xu J, Wang Y, Tu F, Gill PS, Ha T, Liu L, Williams DL, Li C. Lactate promotes macrophage HMGB1 lactylation, acetylation, and exosomal release in polymicrobial sepsis. Cell Death Differ. 2022 Jan;29(1):133-146.
Ge X, Desert R, Magdaleno F, Han H, Song Z, Das S, Athavale D, Chen W, Barahona I, Lantvit D, Chen H, Hwang S, Nieto N. Redox-sensitive high-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice. J Hepatol. 2024 Mar;80(3):482-494.
Chen R, Zou J, Liu J, Kang R, Tang D. DAMPs in the immunogenicity of cell death. Mol Cell. 2025 Oct 16;85(20):3874-3889.
Strain Strategy
The sequences from the 5’UTR to the 3’UTR of the mouse Ager gene were replaced with the sequences from the 5’UTR to the 3’UTR of the human AGER gene. The p.G82S (GGC to AGC) is the most described SNP within the human AGER gene. And the G allele frequency is much higher than the A allele, so we used the G allele at the SNP site.
Figure 1. Gene editing strategy of huRAGE(AGER)(BALB/c) mice.
Application Area
Study the pathogenic mechanism of the human RAGE-AGEs axis in vascular inflammation, plaque formation and cardiovascular events;
Explore the role of human RAGE-mediated Aβ transport and neuroinflammation in the pathogenesis of Alzheimer's disease and corresponding intervention strategies;
Evaluate the alleviating effect of blocking human RAGE signal on the systemic inflammatory response and multi-organ damage induced by damage-associated molecular patterns (DAMPs) such as HMGB1;
Investigate the mechanism by which human RAGE promotes epithelial cell activation and fibrosis in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD);
Evaluate the pharmacological efficacy and safety of human RAGE-targeting therapeutics.
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