C57BL/6NCya-Vtnem1/Cya
Common Name:
Vtn-KO
Product ID:
S-KO-05726
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Vtn-KO
Strain ID
KOCMP-22370-Vtn-B6N-VA
Gene Name
Product ID
S-KO-05726
Gene Alias
Vn
Background
C57BL/6NCya
NCBI ID
Modification
Conventional knockout
Chromosome
11
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Vtnem1/Cya mice (Catalog S-KO-05726) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000017488
NCBI RefSeq
NM_011707
Target Region
Exon 3~6
Size of Effective Region
~1.1 kb
Detailed Document
Overview of Gene Research
Vtn, also known as Vitronectin, is a protein-encoding gene. Vitronectin is involved in multiple biological processes, including cell-cell and cell-extracellular matrix (ECM) interactions, and may participate in signaling pathways related to phagocytosis, fibroblast activation, and immune responses [1,2,3]. Its study using genetic models like knockout mice can help reveal its in-vivo functions.
In tumor research, a genome-wide CRISPR screen identified Vtn as part of a ligand-receptor pair (Vtn-C1qbp) that inhibits macrophage phagocytosis of tumor cells. Tumor cell-secreted Vtn interacts with C1qbp on tumor-associated macrophages, shifting macrophages towards the M2-like subtype. Knockdown of Vtn enhanced macrophage phagocytosis and infiltration, reducing tumor growth in mouse models, suggesting it as a new anti-phagocytic signal in tumors [1].
In kidney fibrosis, Vtn was upregulated in fibrotic kidneys and primarily secreted by activated macrophages. Genetic Vtn knockout (Vtn-/-) mice were protected from developing kidney fibrosis after injury, while overexpression of Vtn exacerbated renal fibrotic lesions. Macrophage-derived Vtn-enriched ECM promoted fibroblast activation via integrin αvβ5 and Src kinase signaling [2].
In the context of idiopathic pulmonary fibrosis, knockdown of FBLN2, which binds to VTN, suppressed TGF-β1-induced MRC-5 cell migration and fibrosis by downregulating VTN, and overexpression of VTN partly abolished these inhibitory effects [4].
In conclusion, Vtn plays essential roles in tumor progression, kidney fibrosis, and pulmonary fibrosis. The use of Vtn knockout or knockdown models in mice has been crucial in understanding its functions in these disease areas, highlighting its potential as a therapeutic target for triple-negative breast cancer, fibrotic chronic kidney disease, and idiopathic pulmonary fibrosis [1,2,4].
References:
1. Zhang, Chen, Liu, Yi, Jiang, Jiayu, Xiang, Rong, Luo, Yunping. 2024. Targeting tumor cell-to-macrophage communication by blocking Vtn-C1qbp interaction inhibits tumor progression via enhancing macrophage phagocytosis. In Theranostics, 14, 2757-2776. doi:10.7150/thno.94537. https://pubmed.ncbi.nlm.nih.gov/38773982/
2. Peng, Yiling, Li, Li, Shang, Jingyue, Fu, Haiyan, Liu, Youhua. 2023. Macrophage promotes fibroblast activation and kidney fibrosis by assembling a vitronectin-enriched microenvironment. In Theranostics, 13, 3897-3913. doi:10.7150/thno.85250. https://pubmed.ncbi.nlm.nih.gov/37441594/
3. Rai, Alin, Fang, Haoyun, Claridge, Bethany, Simpson, Richard J, Greening, David W. . Proteomic dissection of large extracellular vesicle surfaceome unravels interactive surface platform. In Journal of extracellular vesicles, 10, e12164. doi:10.1002/jev2.12164. https://pubmed.ncbi.nlm.nih.gov/34817906/
4. Zhang, Yanju, Zhang, Weishuai, Zhang, Rui, Xia, Yunfei. 2022. Knockdown of FBLN2 suppresses TGF-β1-induced MRC-5 cell migration and fibrosis by downregulating VTN. In Tissue & cell, 81, 102005. doi:10.1016/j.tice.2022.102005. https://pubmed.ncbi.nlm.nih.gov/36608640/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen