huGPAM Mouse
Product Name
huGPAM Mouse
Product ID
C002018
Strain Name
C57BL/6NCya-Gpamtm1(hGPAM)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “huGPAM Mouse (Catalog C002018) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
GPAM
Gene Alias
GPAT, GPAT1
NCBI ID
Chromosome
Chr 10 (Human)
MGI ID
Datasheet
Strain Description
GPAM (Glycerol-3-phosphate acyltransferase, mitochondrial) is a mitochondrial outer membrane-associated acyltransferase and one of the key rate-limiting enzymes involved in triglyceride biosynthesis, primarily expressed in metabolic tissues including the liver and adipose tissue [1-2]. GPAM participates in triglyceride and phospholipid synthesis, lipid storage, and energy metabolism regulation, and is closely associated with mitochondrial homeostasis and lipid metabolic reprogramming [2-3]. Studies have shown that aberrant GPAM expression or dysfunction is associated with the pathogenesis of metabolic disorders, including Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Metabolic Dysfunction-Associated Steatohepatitis (MASH), obesity, and insulin resistance. Therefore, GPAM is considered a potential therapeutic target for metabolic diseases, and studies on GPAM inhibitors and related mechanisms have been conducted [3-4].
The huGPAM mouse is a humanized model generated by replacing the sequences from the start codon to downstream of the 3'UTR of the mouse Gpam gene with the sequences from the start codon to downstream of the 3'UTR of the human GPAM gene. This model can be used for in vivo pharmacodynamic and safety evaluation of GPAM-targeted candidate therapeutics and is also applicable for studies of the pathogenesis and progression of metabolic disorders, including Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Metabolic Dysfunction-Associated Steatohepatitis (MASH), obesity, and lipid metabolism disorders, as well as lipid metabolic regulatory networks and combination therapeutic strategies.
Reference
Yet S F, Lee S, Hahm Y T, et al. Mitochondrial glycerol-3-phosphate acyltransferase expression in human tissues and its functional characterization[J]. Biochemical Journal, 1998, 331(Pt 3): 809-816.
Hammond L E, Gallagher P A, Wang S, et al. Mitochondrial glycerol-3-phosphate acyltransferase-deficient mice have reduced weight and liver triacylglycerol content and altered glycerolipid fatty acid composition[J]. Molecular and Cellular Biology, 2002, 22(23): 8204-8214.
Lewin T M, Wang P, Coleman R A. Analysis of amino acid motifs diagnostic for the sn-glycerol-3-phosphate acyltransferase reaction[J]. Biochemistry, 1999, 38(18): 5764-5771.
Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome[J]. Hepatology, 2003, 37(4): 917-923.
Strain Strategy
The sequences from the start codon to downstream of the 3'UTR of the mouse Gpam gene were replaced with the sequences from the start codon to downstream of the 3'UTR of the human GPAM gene.
Figure 1. Gene editing strategy of huGPAM mice.
Application Area
Research on lipid metabolism and energy homeostasis regulation;
Study of pathogenesis and drug evaluation for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Metabolic Dysfunction-Associated Steatohepatitis (MASH);
Research on obesity, insulin resistance, and type 2 diabetes;
Targeted drug screening and efficacy evaluation for triglyceride synthesis-related metabolic pathways;
Functional study of mitochondrial glycerol-3-phosphate acyltransferase.
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