Korea University · Medicine
Professor Seong-Mi Park's research lab focuses on molecular mechanisms underlying cancer progression and treatment resistance, with a central emphasis on signaling pathways involving NF-κB, p53, mTOR, and RIP1. The lab investigates how key regulatory proteins such as receptor-interacting protein 1 (RIP1) modulate tumor suppressor functions and oncogenic signaling, particularly in glioblastoma and other malignancies. Additional research explores translational control via internal ribosomal entry sites (IRES) and their role in viral and cellular gene expression. The lab also examines cardiovascular implications of molecular signaling, including arterial stiffness and endothelial dysfunction in hypertension.
Figures are computed from collected data and may differ slightly.
CRD42020198152.
Nuclear factor-kappaB (NF-kappaB) activation may play an important role in the pathogenesis of cancer and also in resistance to treatment. Inactivation of the p53 tumor suppressor is a key component of the multistep evolution of most cancers. Links between the NF-kappaB and p53 pathways are under intense investigation. In this study, we show that the receptor interacting protein 1 (RIP1), a central component of the NF-kappaB signaling network, negatively regulates p53 tumor suppressor signaling.
Therapeutic inhibition of mammalian target of rapamycin (mTOR) in cancer is complicated by the existence of a negative feedback loop linking mTOR to the phosphatidylinositol 3-kinase (PI3K)-Akt pathway. Thus, mTOR inhibition by rapamycin or TSC1/2 results in increased PI3K-Akt activation. The death domain kinase receptor interacting protein 1 (RIP1) plays a key role in nuclear factor-kappaB (NF-kappaB) activation and also activates the PI3K-Akt pathway through unknown mechanisms. RIP1 has recent
It is feasible and useful to use the ASI for detection of atherosclerotic coronary disease. The findings of ASI-H suggests that in addition to stiffening of the arterial wall itself, the impairment of flow mediated vasodilation, because of endothelial dysfunction, further increases the arterial stiffness.
The number of young adults with hypertension (HT) is increasing. We investigated the changes of left ventricular (LV) function and their relationship to the ambulatory blood pressure monitoring (ABPM) parameters in young adults with never-treated HT and no LV hypertrophy. Consecutive young patients (29.5 ± 5.9 years) with first diagnosed primary HT and sex- and age-matched normotensive controls were enrolled. We excluded patients who had LV hypertrophy. ABPM was performed in all HT patients. LV
Translation of many cellular and viral mRNAs is directed by internal ribosomal entry sites (IRESs). Several proteins that enhance IRES activity through interactions with IRES elements have been discovered. However, the molecular basis for the IRES-activating function of the IRES-binding proteins remains unknown. Here, we report that NS1-associated protein 1 (NSAP1), which augments several cellular and viral IRES activities, enhances hepatitis C viral (HCV) IRES function by facilitating the forma
Myocardial deformation assessed by 2DS was related to myocardial fibrosis assessed by IBS. LV reverse remodelling was predicted by mean CVIBS and GCS in patients with non-ischaemic DCM and GCS assessed by 2DS imaging is a simple method and therefore it can be readily used in clinical practice.
We suggest that analysis of VTCs in 16 segments using RT3DE may be a useful alternative to TDI for the evaluation of LV asynchrony.
Open papers in the app to read, cite, and organize with AI.
