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- ● Diet-Induced Obesity (DIO) Mouse Model
- ● Type 1 Diabetes Mellitus (T1DM) Mouse Model
- ● Type 2 Diabetes Mellitus (T2DM) Mouse Model
- ● Diet-induced Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Mouse Model
- ● Chemically Induced Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Mouse Model
- ● Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Mouse Model (Gene-editing)
- ● Composite (Combined) Model - Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Model
- ● Composite Model - Atherosclerosis Mouse Model
- ● Atherosclerosis Mouse Model (Gene-editing)
- ● Acute Pancreatitis Mouse Model
- ● Chronic Pancreatitis Mouse Model
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hF11 Mice
Catalog Number: C001272
Strain Name: C57BL/6NCya-F11tm1(hF11)/Cya
Genetic Background: C57BL/6NCya
Reproduction: Homozygote x Homozygote
Strain Description
The F11 gene encodes coagulation factor XI of the blood coagulation cascade. This protein is present in plasma as a zymogen, a unique plasma coagulation enzyme because it is a homodimer consisting of two identical polypeptide chains linked by disulfide bonds. During activation of the plasma factor XI, an internal peptide bond is cleaved by factor XIIa (or XII) in each of the two chains, resulting in activated factor XIa, a serine protease composed of two heavy and two light chains held together by disulfide bonds. This activated plasma factor XI triggers the middle phase of the intrinsic pathway of blood coagulation by activating factor IX. Defects in this factor lead to Rosenthal syndrome, a blood coagulation abnormality.
This strain is a humanized model of F11 in which the CDS of human F11 (hF11) is expressed under the regulation of the mouse endogenous F11 gene promoter, and the expression of the mouse F11 gene is disrupted to reduce cross-reactivity. This model can be used for in vivo efficacy assessment and analysis of diseases associated with human F11, and homozygous hF11 mice are viable and fertile.
Strain Strategy
Figure 1. Diagram of the gene editing strategy for the generation of hF11 mice. The “human F11 CDS plus 3'UTR” gene expression element was inserted downstream of the mouse endogenous F11 gene promoter by gene editing technology.
Application
- Research on Rosenthal syndrome;
- Research on the intrinsic pathway of blood coagulation.
Validation Data
1. Coagulation tetrad test
Figure 1. Coagulation tetrad test in wild-type (WT) and hF11 mice. The results show that there are no significant differences in prothrombin time (PT), fibrinogen (FIB), and thrombin time (TT) between female hF11 mice and wild-type mice. Although the activated partial thromboplastin time (APTT) in female hF11 mice shows considerable individual variation, it is not statistically different from that of wild-type mice. In male hF11 mice, there are no significant differences in prothrombin time (PT) and activated partial thromboplastin time (APTT) compared to wild-type mice; however, the thrombin time (TT) is prolonged, and the fibrinogen (FIB) content is decreased in male hF11 mice.
