Ji-ha Choi
Ewha Womans University · Biochemistry, Genetics and Molecular Biology
About the Lab
Professor Ji-ha Choi's research lab focuses on molecular mechanisms underlying human diseases, particularly those involving membrane transport proteins and their genetic variants. The lab investigates the functional impacts of genetic polymorphisms and mutations in genes such as CFTR, ABCB4 (MDR3), and MATE1, with a strong emphasis on their roles in cystic fibrosis, cholestatic liver diseases, and drug disposition. Using molecular, cellular, and in vivo models, the lab explores regulatory pathways involving transcription factors (e.g., AP-1, AP-2, STAT6) and post-translational mechanisms like autophagy-mediated protein clearance, especially in metabolic and inflammatory diseases. A central theme is translating genetic and biochemical findings into novel therapeutic strategies for complex disorders such as obesity-related cardiomyopathy and chronic inflammatory conditions.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Aberrant membrane transport caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is associated with a wide spectrum of respiratory and digestive diseases as well as cystic fibrosis. Using a gene scanning method, we found 11 polymorphisms and mutations of the CFTR gene in the Korean population. Individual variants at these sites were analyzed by conventional DNA screening in 117 control and 75 patients having bronchiectasis or chronic pancreatitis. In a haplo
POR variants affect CYP3A4 activities. The impact of a POR variant on catalysis by CYP3A4 is substrate-specific, probably because of substrate-induced conformational changes in CYP3A4.
Our study suggests that the rate of transcription of MATE1 is regulated by AP-1 and AP-2rep and that a common promoter variant, g.-66T>C may affect the expression level of MATE1 in human kidney, and ultimately result in variation in drug disposition and response.
These results provide clear evidence of the critical role of modulating cardiac LPL activity through autophagy-mediated proteolytic clearance as a potential novel strategy to overcome obesity-related cardiomyopathy.
The signal transducer and activator of transcription 6 (STAT6) transcription factor promotes activation of the peroxisome proliferator-activated receptor gamma (PPARγ) pathway in macrophages. Little is known about the effect of proximal signal transduction leading to PPARγ activation for the resolution of acute inflammation. Here, we studied the role of STAT6 signaling in PPARγ activation and the resolution of acute sterile inflammation in a murine model of zymosan-induced peritonitis. First, we
Multidrug resistance 3 (MDR3), encoded by the ATP-binding cassette, subfamily B, member 4 gene (ABCB4), localizes to the canalicular membrane of hepatocytes and translocates phosphatidylcholine from the inner leaflet to the outer leaflet of the canalicular membrane. Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare hepatic disease caused by genetic mutations of ABCB4. In this study, we characterized 8 ABCB4 mutations found in PFIC3 patients, using in vitro molecular assays.
Imbalance in the antioxidant defense system leads to detrimental consequences, such as neurological disorders. The Nrf2 signaling is known as a main pathway involved in cellular defense system. Nrf2 is a transcription factor that regulates oxidative stress response by inducing expression of various antioxidant enzyme genes. In this study, we screened several pure natural compounds for Nrf2 activator. Among them, shizukahenriol (SZH), isolated from Chloranthus henryi, activated Nrf2, and induced
Our study suggests that common promoter haplotypes of MATE2-K are associated with the pharmacokinetics of metformin.
Research Areas
Dive deeper into Ji-ha Choi's research on Nubint
Open this lab's papers in the app to read with AI, summarize, and cite in your writing.