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      • KCI등재

        Xanthogranulomatous inflammation of the lower jaw bone: a rare case report

        Hyesung Bae,Kil-Hwa Yoo,Min-Seok Oh 대한구강악안면외과학회 2023 대한구강악안면외과학회지 Vol.49 No.6

        Xanthogranulomatous inflammation (XGI) is an uncommon type of chronic inflammation and is histologically characterized by foamy histiocytes and giant cells. The most common sites of occurrence are kidneys and gallbladder. The etiology remains controversial. Involvement of the lower jaw bone is rare. In this study, we report a case of XGI presenting in the lower jaw.

      • KCI등재

        Phospholipase D2 is a positive regulator of sirtuin 1 and modulates p53-mediated apoptosis via sirtuin 1

        Lee Hyesung,Jung Taek-Yeol,Lim Seong Hun,Choi Eun Ju,이진우,Min Do Sik 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

        Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent histone deacetylase that plays diverse physiological roles. However, little is known about the regulation of SIRT1 activity. Here, we show that phospholipase D2 (PLD2), but not PLD1, selectively interacts with SIRT1 and increases the deacetylase activity of SIRT1. PLD2 does not interact with the other isozymes of SIRT (SIRT2–7). Two leucine residues in the LXXLL motif (L173 and L174) in the phox domain of PLD2 interact with the region essential for SIRT1 activity. PLD2 stimulates the SIRT1-mediated deacetylation of p53 independent of its lipase activity. In our study, mutagenesis of the LXXLL motif suppressed the interaction of PLD2 with SIRT1 and inhibited SIRT1-mediated p53 deacetylation and p53-induced transactivation of proapoptotic genes. Ultimately, overexpression of wild-type PLD2 but not that of LXXLL-mutant PLD2 protected cells against etoposide-induced apoptosis. Moreover, PLD2 did not protect against apoptosis induced by SIRT1 depletion under genotoxic stress. Collectively, our results suggest that PLD2 is a positive regulator of SIRT1 and modulates p53-mediated apoptosis via SIRT1.

      • Reduction-Sensitive, Robust Vesicles with a Non-covalently Modifiable Surface as a Multifunctional Drug-Delivery Platform

        Park, Kyeng Min,Lee, Don-Wook,Sarkar, Bijay,Jung, Hyuntae,Kim, Jeeyeon,Ko, Young Ho,Lee, Kyung Eun,Jeon, Hyesung,Kim, Kimoon WILEY-VCH Verlag 2010 Small Vol.6 No.13

        <P>The design and synthesis of a novel reduction-sensitive, robust, and biocompatible vesicle (SSCB[6]VC) are reported, which is self-assembled from an amphiphilic cucurbit[6]uril (CB[6]) derivative that contains disulfide bonds between hexaethylene glycol units and a CB[6] core. The remarkable features of SSCB[6]VC include: 1) facile, non-destructive, non-covalent, and modular surface modification using exceptionally strong host–guest chemistry; 2) high structural stability; 3) facile internalization into targeted cells by receptor-mediated endocytosis, and 4) efficient triggered release of entrapped drugs in a reducing environment such as cytoplasm. Furthermore, a significantly increased cytotoxicity of the anticancer drug doxorubicin to cancer cells is demonstrated using doxorubicin-loaded SSCB[6]VC, the surface of which is decorated with functional moieties such as a folate–spermidine conjugate and fluorescein isothiocyanate–spermidine conjugate as targeting ligand and fluorescence imaging probe, respectively. SSCB[6]VC with such unique features can be used as a highly versatile multifunctional platform for targeted drug delivery, which may find useful applications in cancer therapy. This novel strategy based on supramolecular chemistry and the unique properties of CB[6] can be extended to design smart multifunctional materials for biomedical applications including gene delivery.</P> <B>Graphic Abstract</B> <P>Biocompatible vesicles based on cucurbit[6]uril (CB[6]) can undergo surface modification by host–guest chemistry, internalization into targeted cells by receptor-mediated endocytosis, and triggered release of entrapped drugs in cytoplasm. They serve as a highly versatile multifunctional platform for targeted drug delivery. <img src='wiley_img_2010/16136810-2010-6-13-SMLL201000293-content.gif' alt='wiley_img_2010/16136810-2010-6-13-SMLL201000293-content'> </P>

      • Heart rate variability associated with posttraumatic stress disorder in victims’ families of sewol ferry disaster

        Lee, Sang Min,Han, Hyesung,Jang, Kuk-In,Huh, Seung,Huh, Hyu Jung,Joo, Ji-Young,Chae, Jeong-Ho Elsevier 2018 Psychiatry Research Vol.259 No.-

        <P><B>Abstract</B></P> <P>Posttraumatic stress disorder (PTSD), which is caused by a major traumatic event, has been associated with autonomic nervous function. However, there have been few explorations of measuring biological stress in the victims’ family members who have been indirectly exposed to the disaster. Therefore, this longitudinal study examined the heart rate variability (HRV) of the family members of victims of the Sewol ferry disaster. We recruited 112 family members of victims 18 months after the disaster. Sixty-seven participants were revisited at the 30 months postdisaster time point. HRV and psychiatric symptoms including PTSD, depression and anxiety were evaluated at each time point. Participants with PTSD had a higher low frequency to high frequency ratio (LF:HF ratio) than those without PTSD. Logistic regression analysis showed that the LF:HF ratio at 18 months postdisaster was associated with a PTSD diagnosis at 30 months postdisaster. These results suggest that disrupted autonomic nervous system functioning for longer than a year after trauma exposure contributes to predicting PTSD vulnerability. Our finding may contribute to understand neurophysiologic mechanisms underlying secondary traumatic stress. Future studies will be needed to clarify the interaction between autonomic regulation and trauma exposure.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We investigated the association between HRV and PTSD in victims’ family members. </LI> <LI> Victims’ family members with PTSD exhibited higher LF:HF ratio than those without PTSD. </LI> <LI> LF:HF ratio at 18 months postdisaster was associated with PTSD at 30 months postdisaster. </LI> </UL> </P>

      • KCI등재

        PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways

        Lim Seong Hun,Lee Hyesung,Lee Hyun Ji,Kim Kuglae,Choi Junjeong,Han Jung Min,Min Do Sik 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-

        The development of chemoresistance is a major challenge in the treatment of several types of cancers in clinical settings. Stemness and chemoresistance are the chief causes of poor clinical outcomes. In this context, we hypothesized that understanding the signaling pathways responsible for chemoresistance in cancers is crucial for the development of novel targeted therapies to overcome drug resistance. Among the aberrantly activated pathways, the PI3K-Akt/Wnt/β-catenin signaling pathway is clinically implicated in malignancies such as colorectal cancer (CRC) and glioblastoma multiforme (GBM). Aberrant dysregulation of phospholipase D (PLD) has been implicated in several malignancies, and oncogenic activation of this pathway facilitates tumor proliferation, stemness, and chemoresistance. Crosstalk involving the PLD and Wnt/β-catenin pathways promotes the progression of CRC and GBM and reduces the sensitivity of cancer cells to standard therapies. Notably, both pathways are tightly regulated and connected at multiple levels by upstream and downstream effectors. Thus, gaining deeper insights into the interactions between these pathways would help researchers discover unique therapeutic targets for the management of drug-resistant cancers. Here, we review the molecular mechanisms by which PLD signaling stimulates stemness and chemoresistance in CRC and GBM. Thus, the current review aims to address the importance of PLD as a central player coordinating cross-talk between the PI3K/Akt and Wnt/β-catenin pathways and proposes the possibility of targeting these pathways to improve cancer therapy and overcome drug resistance.

      • Probing sub-diffraction optical confinement <i>via</i> the polarized Raman spectroscopy of a single-walled carbon nanotube

        Kim, Yun-Tae,Min, Hyegi,Lee, Junghyun,Park, Hyesung,Lee, Chang Young The Royal Society of Chemistry 2018 Nanoscale Vol.10 No.3

        <P>Polarized Raman spectroscopy of a single-walled carbon nanotube (SWNT) was shown to serve as a simple alternative to sophisticated imaging tools for probing sub-diffraction optical phenomena. As a model system, we used TiO2 nanoparticles (<I>n</I> ∼ 2.67), which confine plane-polarized incident light (<I>λ</I> = 532 nm) into two bands less than 150 nm apart. After depositing the nanoparticles onto SWNTs and measuring the nanoparticle-SWNT distance, Raman spectra of individual SWNTs were obtained with the excitation laser polarized either parallel (<I>θ</I> = 0°) or perpendicular (<I>θ</I> = 90°) to the nanotubes. The spectral intensity increased by the nanoparticles only at <I>θ</I> = 90°, with the degree of enhancement being greater when the nanotube was located farther from the particle-substrate contact. Finite-difference time-domain simulations explained that such an enhancement at <I>θ</I> = 90° was a sub-diffraction phenomenon, which occurred when the nanotubes were located within one of the two confined bands formed by the TiO2 nanoparticles. On repeating the measurements on a two-dimensional graphene sheet, only diminished Raman scattering of the graphene with no polarization dependence was observed, confirming the advantage of the one-dimensional nanostructure for studying sub-diffraction optics.</P>

      • SCIEKCI등재

        Analysis of OsmiR399 expression and down-regulation of LTN1 by the multiple members of OsmiR399 family in rice

        Kwon, Eun Ji,Lee, Min Kyoung,Jeon, Hyesung,Hwang, Jae Min,Kim, Ju-Kon,Kim, Minkyun The Korean Society for Applied Biological Chemistr 2016 Applied Biological Chemistry (Appl Biol Chem) Vol.59 No.4

        Among the many miRNAs involved in plant stress responses, miR399 is well known to be involved in controlling phosphate homeostasis by down-regulating the expression of PHO2, which encodes the ubiquitin-conjugating E2 enzyme, UBC24, in Arabidopsis. In this study, to understand the expression of the rice OsmiR399 genes under abiotic stress conditions, the expression of the eleven OsmiR399 (a-k) genes was studied by analyzing the levels of their precursor transcripts (pre-miRNAs) in the roots and shoots of rice seedlings subjected to the stress-responsive phytohormone abscisic acid (ABA). We found that the OsmiR399 genes showed different patterns in pre-miRNA accumulation. In particular, OsmiR399b, OsmiR399d, OsmiR399e, and OsmiR399f showed high and steady accumulation in both the roots and shoots regardless of ABA treatments. However, OsmiR399c and OsmiR399k showed ABA-induced expression in the whole plant body or aerial part of the rice seedlings. In addition, to test the possibility that the putative rice PHO2 ortholog of Arabidopsis, also known as LEAF TIP NECROSIS 1 (LTN1), might be down-regulated by the multiple OsmiR399s with certain sequence divergences, four different lines of transgenic rice plants that overexpress either the constitutively expressed OsmiR399s (OsmiR399d and OsmiR399f) or the ABA-inducible OsmiR399s (OsmiR399c and OsmiR399k) were produced and the levels of OsmiR399 pre-miRNAs and LTN1 transcripts were analyzed. A significant decrease in the accumulation of LTN1 transcripts and an increase in the OsmiR399 pre-miRNAs levels were found in all of the transgenic plants. Based on these results, we concluded that LTN1 is down-regulated by multiple OsmiR399 genes in rice.

      • KCI등재

        Inhibition of phospholipase D1 induces immunogenic cell death and potentiates cancer immunotherapy in colorectal cancer

        Hwang Won Chan,Song Doona,Lee Hyesung,Oh Changmok,Lim Seong Hun,Bae Hyeon Jeong,Kim Namdoo,Han Gyoonhee,Min Do Sik 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

        Phospholipase D (PLD) is a potential therapeutic target against cancer. However, the contribution of PLD inhibition to the antitumor response remains unknown. We developed a potent and selective PLD1 inhibitor based on computer-aided drug design. The inhibitor enhanced apoptosis in colorectal cancer (CRC) cells but not in normal colonic cells, and in vitro cardiotoxicity was not observed. The inhibitor downregulated the Wnt/β-catenin signaling pathway and reduced the migration, invasion, and self-renewal capacity of CRC cells. In cancer, therapeutic engagement of immunogenic cell death (ICD) leads to more effective responses by eliciting the antitumor immunity of T cells. The CRC cells treated with the inhibitor showed hallmarks of ICD, including downregulation of “do not eat-me” signals (CD24, CD47, programmed cell death ligand 1 [PD-L1]), upregulation of “eat-me” signal (calreticulin), release of high-mobility group Box 1, and ATP. PLD1 inhibition subsequently enhanced the phagocytosis of cancer cells by macrophages through the surface expression of costimulatory molecules; as a result, the cancer cells were more susceptible to cytotoxic T-cell-mediated killing. Moreover, PLD1 inhibition attenuated colitis-associated CRC and orthotopically injected tumors, probably by controlling multiple pathways, including Wnt signaling, phagocytosis checkpoints, and immune signaling. Furthermore, combination therapy with a PLD1 inhibitor and an anti-PD-L1 antibody further enhanced tumor regression via immune activation in the tumor environment. Collectively, in this study, PLD1 was identified as a critical regulator of the tumor microenvironment in colorectal cancer, suggesting the potential of PLD1 inhibitors for cancer immunotherapy based on ICD and immune activation. PLD1 inhibitors may act as promising immune modulators in antitumor treatment via ICD.

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