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Kim, Youngsoo,Kim, Seong Hun,Kim, Kook Hwan,Chae, Sujin,Kim, Chanki,Kim, Jeongjin,Shin, Hee-Sup,Lee, Myung-Shik,Kim, Daesoo IRL Press 2015 Human molecular genetics Vol.24 No.25
<P>Really interesting new gene (RING) finger protein 170 (RNF170) is an E3 ubiquitin ligase known to mediate ubiquitination-dependent degradation of type-I inositol 1,4,5-trisphosphate receptors (ITPR1). It has recently been demonstrated that a point mutation of <I>RNF170</I> gene is linked with autosomal-dominant sensory ataxia (ADSA), which is characterized by an age-dependent increase of walking abnormalities, a rare genetic disorder reported in only two families. Although this mutant allele is known to be dominant, the functional identity thereof has not been clearly established. Here, we generated mice lacking <I>Rnf170</I> (<I>Rnf170<SUP>−/−</SUP></I>) to evaluate the effect of its loss of function <I>in vivo</I>. Remarkably, <I>Rnf170<SUP>−/−</SUP></I> mice began to develop gait abnormalities in old age (12 months) in the form of asynchronous stepping between diagonal limb pairs with a fixed step sequence during locomotion, while age-matched wild-type mice showed stable gait patterns using several step sequence repertoires. As reported in ADSA patients, they also showed a reduced sensitivity for proprioception and thermal nociception. Protein blot analysis revealed that the amount of Itpr1 protein was significantly elevated in the cerebellum and spinal cord but intact in the cerebral cortex in <I>Rnf170<SUP>−/−</SUP></I> mice. These results suggest that the loss of <I>Rnf170</I> gene function mediates ADSA-associated phenotypes and this gives insights on the cure of patients with ADSA and other age-dependent walking abnormalities.</P>
Kim, Ji Sung,Park, Yun Soo,Kim, Ju Young,Kim, Yong Guk,Kim, Yeon Jin,Lee, Hong Kyung,Kim, Hyung Sook,Hong, Jin Tae,Kim, Youngsoo,Han, Sang-Bae The Korean Association of Immunobiologists 2012 Immune Network Vol.12 No.6
Pancreatic cancer is the fourth commonest cause of cancer-related deaths in the world. However, no adequate therapy for pancreatic cancer has yet been found. In this study, the antitumor activity of cytokine-induced killer (CIK) cells against the human pancreatic cancer was evaluated in vitro and in vivo. Human peripheral blood mononuclear cells were cultured with IL-2-containing medium in anti-CD3 for 14 days. The resulting populations of CIK cells comprised 94% $CD3^+$, 4% $CD3^-CD56^+$, 41% $CD3^+CD56^+$, 11% $CD4^+$, and 73% $CD8^+$. This heterogeneous cell population was called cytokine-induced killer (CIK) cells. At an effector-target cell ratio of 100 : 1, CIK cells destroyed 51% of AsPC-1 human pancreatic cancer cells, as measured by the $^{51}Cr$-release assay. In addition, CIK cells at doses of 3 and 10 million cells per mouse inhibited 42% and 70% of AsPC-1 tumor growth in nude mouse xenograft assays, respectively. This study suggests that CIK cells may be used as an adoptive immunotherapy for pancreatic cancer patients.
Real-time imaging of glioblastoma using bioluminescence in a U-87 MG xenograft model mouse
Kim, Woong,Kang, Bo Ram,Kim, Hye Yun,Cho, Soo Min,Lee, Yong-Deok,Kim, Sehoon,Kim, Jung Young,Kim, Dong Jin,Kim, YoungSoo The Korean Society for Applied Biological Chemistr 2015 Applied Biological Chemistry (Appl Biol Chem) Vol.58 No.2
Glioblastoma multiforme (GBM), the most common malignant brain tumor, is characterized by aggressive proliferation and invasive potential. Xenograft animal models of GBM have critically contributed to evaluation of novel therapeutic agents, drug delivery system, and diagnostic tools. To mimic intrinsic behavior of GBM, orthotopic transplantation of cancer cells and continuous observation of cell growth should be conducted in animal study. Here, we generated xenograft model mouse of GBM in which U-87 MG human glioblastoma cells were intracranially implanted for live imaging. Introducing luciferase gene into U-87 MG cell line enabled real-time observation and quantification of tumor survival and propagation by detecting photon emission derived from luciferase. Our GBM model mouse has potentials to bring great advantages in pharmacological and mechanistic investigation on brain tumors.
Profiling of vitreous proteomes from proliferative diabetic retinopathy and nondiabetic patients
Kim, Taeoh,Kim, Sang Jin,Kim, Kyunggon,Kang, Un-Beom,Lee, Cheolju,Park, Kyong Soo,Yu, Hyeong Gon,Kim, Youngsoo WILEY-VCH 2007 Proteomics Vol. No.
<P>Diabetes can lead to serious microvascular complications like proliferative diabetic retinopathy (PDR), which is the leading cause of blindness in adults. The proteomic changes that occur during PDR cannot be measured in the human retina for ethical reasons, but could be reflected by proteomic changes in vitreous humor. Thus, we considered that comparisons between the proteome profiles of the vitreous humors of PDR and nondiabetic controls could lead to the discovery of novel pathogenic proteins and clinical biomarkers. In this study, the authors used several proteomic methods to comprehensively examine vitreous humor proteomes of PDR patients and nondiabetic controls. These methods included immunoaffinity subtraction (IS)/2-DE/MALDI-MS, nano-LC-MALDI-MS/MS, and nano-LC-ESI-MS/MS. The identified proteins were subjected to the Trans-Proteomic Pipeline validation process. Resultantly, 531 proteins were identified, i.e., 415 and 346 proteins were identified in PDR and nondiabetic control vitreous humor samples, respectively, and of these 531 proteins, 240 were identified for the first time in this study. The PDR vitreous proteome was also found to contain many proteins possibly involved in the pathogenesis of PDR. The proteins described provide the most comprehensive proteome listing in the vitreous humor samples of PDR and nondiabetic control patients.</P>
Characterization of morphological changes of B16 melanoma cells under natural killer cell attack
Kim, Ji Sung,Kim, Boyeong,Lee, Hong Kyung,Kim, Hyung Sook,Park, Eun Jae,Choi, Yeo Jin,Ahn, Gi Beom,Yun, Jieun,Hong, Jin Tae,Kim, Youngsoo,Han, Sang-Bae Elsevier 2019 INTERNATIONAL IMMUNOPHARMACOLOGY Vol.67 No.-
<P><B>Abstract</B></P> <P>Natural killer (NK) cell killing of melanoma cells involves perforin-mediated delivery of granzymes from NK cells to cancer cells; however, how melanoma cells die remains poorly characterized. Here, we examined the dying process of melanoma cells by using time-lapse imaging. Upon contact with NK cells, B16-F10 cells rounded and most of them showed membrane rupture (98 min); however, B16 parent cells showed writhing and delayed membrane rupture (235 min). This morphological difference depended on the expression levels of myosin regulatory light chain 9 (MYL9) but not activating ligands (CD112, CD155, Rae-1, and MULT-1), SPI, FasL, or PD-L1. Taken together, our data show that melanoma cells show two distinct types of morphological changes upon contact with NK cells and suggest that a strategy to decrease MYL9 expression by melanoma cells may improve the efficacy of NK cell–based immunotherapy.</P>
Amelioration of Alzheimer’s disease by neuroprotective effect of sulforaphane in animal model
Kim, Hyunjin Vincent,Kim, Hye Yun,Ehrlich, Hanna Y.,Choi, Seon Young,Kim, Dong Jin,Kim, YoungSoo Informa UK, Ltd. 2013 Amyloid Vol.20 No.1
<P>Pathophysiological evidences of AD have indicated that aggregation of Aβ is one of the principal causes of neuronal dysfunction, largely by way of inducing oxidative stresses such as free radical formation. We hypothesized that the known antioxidative attribute of SFN could be harnessed in Alzheimer’s treatment. SFN is an indirect, potent antioxidant derived from broccoli that has previously been found to stimulate the Nrf2-ARE pathway and facilitate several other cytoprotective mechanisms. In this study, administration of SFN ameliorated cognitive function of Aβ-induced AD acute mouse models in Y-maze and passive avoidance behavior tests. Interestingly, we found that the therapeutic effect of SFN did not involve inhibition of Aβ aggregation. While the exact mechanism of interaction of SFN in AD has not yet been ascertained, our results suggest that SFN can aid in cognitive impairment and may protect the brain from amyloidogenic damages.</P><P><B>Abbreviations:</B> Aβ, amyloid-β; AD, Alzheimer’s disease; PBS, phosphate buffered saline; DMSO, dimethyl sulfoxide; ROS, reactive oxygen species; SFN, sulforaphane; DMEM, Dulbecco’s modified eagle medium; FBS, fetal bovine serum; ICR, imprinting control region; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; DW, deionized water; ThT, thioflavin T; PA, passive avoidance; ARE, antioxidant response element.</P>
Kim, Byung-Su,Bae, Eunkyung,Kim, Young-Ju,Ahn, Kwang-Sung,Park, Juwon,Rhee, Ji young,Lee, Young Yiul,Kim, Youngsoo,Lee, Dongsoon,Kim, Byoung Kook,Yoon, Sung-Soo RAPID COMMUNICATIONS OF OXFORD LTD 2007 ANTICANCER DRUGS Vol.18 No.6
Although STI571 still plays a key role in the treatment of chronic myeloid leukemia, emergence of resistance to STI571 is a major obstacle to successful outcome. Therefore, new agents that increase the sensitivity of chronic myeloid leukemia cells to STI571 are urgently required. SK-7041 is a novel hybrid synthetic histone deacetylase inhibitor derived from the hydroxamic acid of trichostatin A and pyridyl ring of MS-275. Its cytotoxic effects were examined both as a single agent and in combination with STI571 in acute and chronic myeloid leukemia. SK-7041 exhibited growth inhibition of leukemia cells by downregulation of CDK4, cyclin E and cyclin B1 expression, and by upregulation of p21 expression with subsequent activation of the mitochondria-mediated caspase pathway. SK-7041 showed synergism on growth inhibition, cell cycle arrest and induction of apoptosis in chronic myeloid leukemia (K562) when combined with STI571. The synergistic effect was mediated through the same mechanism as in SK-7041 alone, involving reduction of cyclin D1 and induction of p21. Taken together, our findings suggest that SK-7041 is active against leukemia and offers new prospects for overcoming STI571 resistance in chronic myeloid leukemia.