Our Experts will contact you providing a quote,
information and estimated timeframe to
your project needs.
Custom Models
-
-
-
-
-
-
-
-
- ● 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
-
-
-
-
-
-
-
-
-
Testimonials
"I've been very happy with Cyagen's service so I've been referring a lot of colleagues... thanks for
the
great service."
'- Washington University in St. Louis
> more
> more
Citations
IMMUNITY 47:107 (2017) IF=22.845
You may also be interested in
Fah KO Mice
Product Number：C001273
Genetic Background：C57BL/6JCya
Reproduction：Homozygote x Homozygote
Strain Description
The FAH gene encodes the fumarylacetoacetate hydrolase (FAH) protein, a key enzyme in the tyrosine catabolism pathway. FAH is expressed in many tissues throughout the body but is most abundant in the liver and kidneys. Mutations in the FAH gene can lead to a deficiency in FAH activity, which results in the accumulation of fumarylacetoacetate (FAA) and other toxic metabolites in the body. This can lead to a variety of health problems, including hereditary tyrosinemia type 1 (HT1) [1-2]. HT1 is a rare autosomal recessive genetic disorder that is characterized by a deficiency in FAH activity. Symptoms of HT1 typically appear in early infancy and can include vomiting, diarrhea, jaundice, and failure to thrive. If left untreated, HT1 can lead to severe liver and kidney damage, as well as intellectual disability.
The Fah knockout mouse model is a valuable tool for studying HT1 and has become a workhorse for liver biology and is widely used in liver stem cell and hepatic gene therapy research. Mice with the Fah gene knocked out develop HT1 and die within a few weeks of birth. The mice exhibit many of the same symptoms as human infants with HT1, including vomiting, diarrhea, jaundice, and failure to thrive [3]. The heterozygous Fah KO mice is viable and fertile.
Figure 1. Gene editing strategy of Fah KO mice. The Fah gene is located on mouse chromosome 7, and exons 2-10 of this gene were knocked out using gene editing techniques.
● Research on tyrosinemia type 1 (HT1).
● Research on liver stem cell and hepatic gene therapy.
● Research on liver repopulation.
References
[1] Morrow G, Angileri F, Tanguay RM. Molecular Aspects of the FAH Mutations Involved in HT1 Disease. Adv Exp Med Biol. 2017;959:25-48.
[2] Frequent mutation reversioninversely correlates with clinical severity in a genetic liver disease,hereditary tyrosinemia.
[3] Grompe M. Fah Knockout Animals as Models for Therapeutic Liver Repopulation. Adv Exp Med Biol. 2017;959:215-230.
