huANGPTL4(1) Mouse
Product Name
huANGPTL4(1) Mouse
Product ID
C002030
Strain Name
C57BL/6NCya-Angptl4tm1(hANGPTL4)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “huANGPTL4(1) Mouse (Catalog C002030) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
ANGPTL4
Gene Alias
NL2, ARP4, FIAF, HARP, PGAR, HFARP, TGQTL, UNQ171, pp1158
NCBI ID
Chromosome
Chr 19 (Human)
MGI ID
Datasheet
Strain Description
Angiopoietin-like protein 4 (ANGPTL4) is a member of the angiopoietin-like protein family and is highly expressed in metabolically active organs and tissues, such as the liver, adipose tissue, and small intestine [1]. As a physiological inhibitor of lipoprotein lipase (LPL), ANGPTL4 non-covalently binds to and inhibits LPL activity primarily through its N-terminal domain, thereby blocking the peripheral hydrolysis and clearance of triglyceride-rich lipoproteins (e.g., chylomicrons and very-low-density lipoprotein remnants) and participating in the regulation of systemic lipid metabolism and triglyceride homeostasis [2]. Studies have demonstrated that the dysfunction of ANGPTL4 is closely associated with obesity, type 2 diabetes (T2D), hypertriglyceridemia, atherosclerotic cardiovascular disease (ASCVD), metabolic dysfunction-associated steatotic liver disease (MASLD), and microenvironmental remodeling in malignancies such as triple-negative breast cancer, making it an important drug discovery target in metabolic disorders, cardiovascular diseases, and oncology translational medicine [2-5].
The huANGPTL4 mouse is a humanized model developed via gene editing technology, in which the entire sequence of the endogenous mouse Angptl4 gene from the start codon to the stop codon is replaced with the corresponding genomic DNA fragment of the human ANGPTL4 gene. This model is applicable for pathological mechanism studies of lipid metabolism disorders, organ fibrosis, and related malignancies, as well as for the screening, development, and preclinical in vivo evaluation of neutralizing antibodies, small molecule inhibitors, and nucleic acid drugs targeting human ANGPTL4.
Reference
Vahdat-Lasemi F, Farhoudi L, Hosseinikhah SM, Santos RD, Sahebkar A. Angiopoietin-like protein inhibitors: Promising agents for the treatment of familial hypercholesterolemia and atherogenic dyslipidemia. Atherosclerosis. 2025 Jun;405:119235.
Singh AK, Chaube B, Zhang X, Sun J, Citrin KM, Canfrán-Duque A, Aryal B, Rotllan N, Varela L, Lee RG, Horvath TL, Price N, Suárez Y, Fernandez-Hernando C. Hepatocyte-specific suppression of ANGPTL4 improves obesity-associated diabetes and mitigates atherosclerosis in mice. J Clin Invest. 2021 Jul 13;131(17):e140989.
Chua D, Low ZS, Kim JHS, Lee YH, Kiatbumrung R, Somnark P, Xu M, Shi Y, Kaushal G, Vos MIG, Mahadevan A, Hooi N, Raj M, Sviriaeva E, Cui B, Tan S, Kasahara K, Ho CL, Wahli W, Yew KC, Wong SH, Cheung C, Pal M, Zhang R, Chuaypen N, Tangkijvanich P, Cheng HS, Li L, Tan NS. Angptl4 integrates dietary and microbial signals to disrupt gut barrier function in MASH. Nat Commun. 2026 May 22.
Yin D, Fang N, Zhu Y, Bao X, Yang J, Zhang Q, Wang R, Huang J, Wu Q, Ma F, Wei X. Adipocytes-induced ANGPTL4/KLF4 axis drives glycolysis and metastasis in triple-negative breast cancer. J Exp Clin Cancer Res. 2025 Jul 4;44(1):192.
Janssen AWF, Katiraei S, Bartosinska B, Eberhard D, Willems van Dijk K, Kersten S. Loss of angiopoietin-like 4 (ANGPTL4) in mice with diet-induced obesity uncouples visceral obesity from glucose intolerance partly via the gut microbiota. Diabetologia. 2018 Jun;61(6):1447-1458.
Strain Strategy
The sequences from the start codon to the stop codon of the endogenous mouse Angptl4 gene were replaced with the sequences from the start codon to the stop codon of the human ANGPTL4 gene.
Figure 1. Gene editing strategy for huANGPTL4(1) mice.
Application Area
ANGPTL4-targeted drug screening, development, and evaluation;
Research on the metabolic disorders such as hypertriglyceridemia, metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, and type 2 diabetes (T2D);
Research on cardiovascular diseases and associated atherosclerotic lesions;
Research on the pathological mechanisms and tumor microenvironment of certain cancers like triple-negative breast cancer.
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