Nonalcoholic fatty liver disease is caused by several factors including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. TCDD causes lipid accumulation in humans by inducing the Solute Carrier Family 46 Member 3 (SLC46A3) gene expression. To effectively study TCDD-mediated lipid accumulation, research tools such as SLC46A3 knockout cells and animal models are required.
Researchers at the National Cancer Institute (NCI) have developed an SLC46A3 knockout mouse line and demonstrated that TCDD-induced hepatic triglyceride accumulation was significantly reduced in the knockout mice compared to the wild type mice. This reduction in triglyceride accumulation was more pronounced when the mice were fed a high fat diet. The SLC46A3 knockout mouse line is therefore an effective tool to study TCDD-induced lipid accumulation, liver toxicity and nonalcoholic fatty liver disease. As SLC46A3 gene and protein are also associated with other diseases such as breast cancer, prostate cancer, liver cancer, papilloma, glioma, obesity, and SARS, this knockout mouse line may have wide applicability.
The NCI is seeking licensees for the SLC46A3 knockout mouse line.
- Drug screening and development against various diseases such as nonalcoholic fatty liver disease, obesity, liver cancer, SARS, breast cancer, prostate cancer, papilloma, glioma
- Research tool to study SLC46A3’s role in hepatic lipid accumulation or as a solute carrier of the Major Facilitator Superfamily (MFS)
- The only known SLC46A knockout mouse line available
- Effective research tool to study TCDD-mediated liver toxicity leading to nonalcoholic fatty liver disease
Frank J Gonzalez Ph.D. (NCI), Sun Hee Yim Ph.D, Jung-Hwan Kim Ph.D
Kim JH, et al. Lysosomal SLC46A3 modulates hepatic cytosolic copper homeostasis