hOSM Mouse
製品名
hOSM Mouse
製品ID
C001815
系統名
C57BL/6NCya-Osmtm1(hOSM)/Cya
背景情報
C57BL/6NCya
状況
このマウス系統を論文で使用する場合は、「hOSM Mouse（カタログ番号C001815）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
--
NCBI ID
染色体
Chr 22
MGI ID
さらに
系統詳細
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].
The hOSM mouse is a humanized model, constructed by replacing the coding sequences of the endogenous mouse Osm gene with the coding sequences of the human OSM gene. hOSM mice can be used for research into the pathogenesis of inflammatory conditions such as arthritis (rheumatoid and osteoarthritis), inflammatory bowel disease, lung and skin diseases (e.g., psoriasis, asthma), cardiovascular diseases (e.g., atherosclerosis), liver diseases (e.g., fibrosis), various cancers, and bone marrow failure syndromes, as well as for the screening, development, and safety evaluation of OSM-targeted drugs.
参考文献
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.
系統作製戦略
The sequences from the ATG start codon to the TAG stop codon of the endogenous mouse Osm gene will be replaced with the sequences from the ATG start codon to the TAG stop codon of the human OSM gene.
Figure 1. Gene editing strategy of hOSM Mice.
適用分野
OSM-targeted drug screening, development, and evaluation;
Research on the pathological mechanisms and therapeutic approaches of inflammatory diseases, including rheumatoid arthritis (RA), osteoarthritis, and inflammatory bowel disease (IBD);
Research on cardiovascular diseases, including atherosclerosis;
Research on liver diseases, including fibrosis;
Research on various cancers;
Research on the pathological mechanisms and therapeutic approaches of bone marrow failure syndromes.
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