Sungkyunkwan University · Medicine
Professor Sungpil Yoon's research lab focuses on molecular and cellular mechanisms underlying cancer drug resistance and transcriptional regulation in yeast and mammalian systems. Key research directions include the role of P-glycoprotein in multidrug resistance, the modulation of DNA damage and apoptosis by natural compounds like salvianolic acid, and the nuclear translocation and function of SOCS proteins in regulating signaling pathways such as JAK-STAT. The lab also investigates chromatin remodeling and transcriptional activation mechanisms, particularly the recruitment of the SWI/SNF complex by transcription factors like Gcn4p in response to nutrient stress.
Figures are computed from collected data and may differ slightly.
We report a study of the magnetic properties of transition-metal doped Zn1−xTMxO (TM=Mn, Co, Fe). Polycrystalline powder samples were synthesized by both solid-state and liquid-phase reactions. From the Curie–Weiss behavior of susceptibility at high temperatures, it was found that the TM–TM interaction is dominated by antiferromagnetic coupling with effective nearest-neighbor exchange constants J=−90 to −30 K. The magnetization data measured at low temperature as a function field H are fit to a
This is the first study to report that Sal increases DNA damage, and this effect plays an important role in the increased apoptosis caused by Sal. Overall, we demonstrated that the ability of Sal to sensitize cancer cells to the effects of DOX or ETO is associated with an increase in DNA damage and a decrease in anti-apoptotic protein p21 levels. These results may contribute to the development of Sal-based chemotherapy for cancer patients receiving DOX or ETO treatment.
The nucleosome remodeling complex SWI/SNF is a coactivator for yeast transcriptional activator Gcn4p. We provide strong evidence that Gcn4p recruits the entire SWI/SNF complex to its target genes ARG1 and SNZ1 but that SWI/SNF is dispensable for Gcn4p binding to these promoters. It was shown previously that Snf2p/Swi2p, Snf5p, and Swi1p interact directly with Gcn4p in vitro. However, we found that Snf2p is not required for recruitment of SWI/SNF by Gcn4p nor can Snf2p be recruited independently
P-glycoprotein (P-gp) is overexpressed in cancer cells in order to pump out chemotherapeutic drugs, and is one of the major mechanisms responsible for multidrug resistance (MDR). It is important to identify P-gp inhibitors with low toxicity to normal cells in order to increase the efficacy of anti-cancer drugs. Previously, a JAK2 inhibitor CEP-33779 demonstrated inhibitory actions against P-gp and an ability to sensitize drug-resistant cancer cells to treatment. In the present study, we tested a
We investigated the cellular localization of ectopically-expressed CIS, SOCS1, SOCS2 and SOCS3 proteins. We found that SOCS proteins localize to the nucleus where they reduce Stat3 proteins and that the presence of proteasome inhibitors increased SOCS nuclear localization. Our results indicate that increased nuclear localization resulted from increased levels of SOCS proteins in the cytoplasm. Finally, we demonstrate that the same effect occurs with endogenously-expressed SOCS proteins. These ob
Transcription of the arginine biosynthetic gene ARG1 is repressed by the ArgR/Mcm1p complex in arginine-replete cells and activated by Gcn4p, a transcription factor induced by starvation for any amino acid. We show that all four subunits of the arginine repressor are recruited to ARG1 by Gcn4p in cells replete with arginine but starved for isoleucine/valine. None of these proteins is recruited to the Gcn4p target genes ARG4 and SNZ1, which are not regulated by ArgR/Mcm1p. Mcm1p and Arg80p were f
To see if evening primrose oil (EPO) could be more effective in a certain type of atopic dermatitis, we administered EPO to 14 atopic dermatitis patients characterized by itchy dry scaly skin. Furthermore, we measured serum levels of gamma-interferon (IFN-gamma) and IgE in addition to the clinical severity before and after the treatment to find out whether the treatment effect of EPO is related with an immunological mechanism. After the treatment, the extent of the skin lesions and the pruritus
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