BALB/c-huOSM Mouse
Product Name
BALB/c-huOSM Mouse
Product ID
C001855
Strain Name
BALB/cAnCya-Osmtm2(hOSM)/Cya
Backgroud
BALB/cAnCya
Status
When using this mouse strain in a publication, please cite “BALB/c-huOSM Mouse (Catalog C001855) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
OSM
Gene Alias
--
NCBI ID
Chromosome
Chr 22 (Human)
MGI ID
Datasheet
Strain Description
The OSM gene (Oncostatin M) encodes a secreted cytokine, Oncostatin M, which is a pleiotropic protein belonging to the leukemia inhibitory factor/oncostatin-M (LIF/OSM) family. This protein is expressed in various immune cells, including activated T lymphocytes, macrophages, and neutrophils, as well as in other tissues like endothelial cells, osteoblasts, and smooth muscle cells [1]. OSM plays diverse functions, acting as a growth regulator that can inhibit the proliferation of certain tumor cell lines, stimulate proliferation of others (e.g., AIDS-KS cells), and regulate the production of other cytokines like IL-6, G-CSF, and GM-CSF. Its activities are mediated through two receptor complexes: Type I (gp130 and LIFRβ) and Type II (gp130 and OSMRβ), primarily activating the JAK/STAT, MAPK, JNK, and PI3K/AKT signaling pathways [2]. OSM is implicated in a wide array of diseases, contributing to inflammatory conditions such as arthritis (rheumatoid and osteoarthritis), inflammatory bowel disease, lung and skin diseases (e.g., psoriasis, asthma), cardiovascular diseases (e.g., atherosclerosis), and liver diseases (e.g., fibrosis) [3]. It also exhibits a complex role in various cancers, sometimes inhibiting tumor growth in early stages or in specific cell lines, while promoting tumorigenesis, epithelial-mesenchymal transition (EMT), invasion, and metastasis in more advanced cancers like breast, cervical, ovarian, pancreatic, and lung cancers. Deficiency in OSM has also been linked to severe bone marrow failure syndromes [4].
BALB/c-huOSM mice are humanized models constructed by gene-editing technology, in which the sequences from the ATG start codon to the TAG stop codon of the endogenous mouse Osm gene were replaced with the sequences from the ATG start codon to the TAG stop codon of the human OSM gene. This model can be used to study the pathogenesis of inflammatory diseases (such as rheumatoid arthritis, osteoarthritis, and inflammatory bowel disease), lung and skin diseases (such as asthma and psoriasis), cardiovascular diseases (such as atherosclerosis), liver diseases (such as fibrosis), and bone marrow failure syndrome, as well as the development of OSM-targeted drugs.
Reference
Han L, Yan J, Li T, Lin W, Huang Y, Shen P, Ba X, Huang Y, Qin K, Geng Y, Wang H, Zheng K, Liu Y, Wang Y, Chen Z, Tu S. Multifaceted oncostatin M: novel roles and therapeutic potential of the oncostatin M signaling in rheumatoid arthritis. Front Immunol. 2023 Nov 1;14:1258765.
Zhou Y, Stevis PE, Cao J, Ehrlich G, Jones J, Rafique A, Sleeman MW, Olson WC, Franklin MC. Structures of complete extracellular assemblies of type I and type II Oncostatin M receptor complexes. Nat Commun. 2024 Nov 12;15(1):9776.
Wolf CL, Pruett C, Lighter D, Jorcyk CL. The clinical relevance of OSM in inflammatory diseases: a comprehensive review. Front Immunol. 2023 Sep 29;14:1239732.
Garrigue A, Kermasson L, Susini S, Fert I, Mahony CB, Sadek H, Luce S, Chouteau M, Cavazzana M, Six E, Le Bousse-Kerdilès MC, Anginot A, Souraud JB, Cormier-Daire V, Willems M, Sirvent A, Russello J, Callebaut I, André I, Bertrand JY, Lagresle-Peyrou C, Revy P. Human oncostatin M deficiency underlies an inherited severe bone marrow failure syndrome. J Clin Invest. 2025 Jan 23;135(6):e180981.
Strain Strategy
The sequences from the ATG start codon to the TAG stop codon of the endogenous mouse Osm gene were replaced with the sequences from the ATG start codon to the TAG stop codon of the human OSM gene.
Figure 1. Gene editing strategy for BALB/c-huOSM mice.
Application Area
Screening, development, and pre-clinical evaluation of OSM-targeted drugs;
Research on the pathological mechanisms and treatment methods of inflammatory diseases (such as rheumatoid arthritis, osteoarthritis, inflammatory bowel disease, asthma, and psoriasis);
Research on cardiovascular diseases (such as atherosclerosis);
Research on liver diseases (such as fibrosis);
Research on the pathological mechanisms and treatment methods of various cancers;
Research on bone marrow failure syndromes.
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