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Search Results: 1 - 10 of 26989 matches for " Dae Won Kim1 "
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PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression
Duk-Soo Kim2,#, Eun Jeong Sohn1,#, Dae Won Kim1, Young Nam Kim1, Seon Ae Eom1, Ga Hyeon Yoon1, Sung-Woo Cho3, Sang-Hyun Lee1, Hyun Sook Hwang1, Yoon Shin Cho1, Jinseu Park1, Won Sik Eum1,* & Soo Young Choi1,*
BMB Reports , 2012,
Abstract: P18, a member of the INK4 family of cyclin-dependent kinaseinhibitors, is a tumor suppressor protein and plays a key cellsurvival role in a variety of human cancers. Under pathophysiologicalconditions, the INK4 group proteins participate in novelbiological functions associated with neuronal diseases andoxidative stress. Parkinson’s disease (PD) is characterized by loss ofdopaminergic neurons, and oxidative stress is important in itspathogenesis. Therefore, we examined the effects of PEP-1-p18 onoxidative stress-induced SH-SY5Y cells and in a PD mouse model.The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenylpyridinium-induced SH-SY5Y cell death by inhibiting Baxexpression levels and DNA fragmentation. Additionally, PEP-1-p18prevented dopaminergic neuronal cell death in the substantia nigraof a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PDmouse model. These results indicate that PEP-1-p18 may be auseful therapeutic agent against various diseases and is a potentialtool for treating PD.
Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein
Sun Hwa Lee1,#, Dae Won Kim1,#, Seon Ae Eom1, Se-Young Jun1, Meeyoung Park1, Duk-Soo Kim2, Hyung Joo Kwon3, Hyeok Yil Kwon4, Kyu Hyung Han1, Jinseu Park1, Hyun Sook Hwang1, Won Sik Eum1,* & Soo Young Choi1,*
BMB Reports , 2012,
Abstract: We examined that the protective effects of ANX1 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammationin animal models using a Tat-ANX1 protein. Topicalapplication of the Tat-ANX1 protein markedly inhibited TPAinducedear edema and expression levels of cyclooxygenase-2(COX-2) as well as pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha(TNF-α). Also, application of Tat-ANX1 protein significantlyinhibited nuclear translocation of nuclear factor-kappa B(NF-κB) and phosphorylation of p38 and extracellular signalregulatedkinase (ERK) mitogen-activated protein kinase(MAPK) in TPA-treated mice ears. The results indicate thatTat-ANX1 protein inhibits the inflammatory response byblocking NF-κB and MAPK activation in TPA-induced miceears. Therefore, the Tat-ANX1 protein may be useful as atherapeutic agent against inflammatory skin diseases.
Human milk oligosaccharides: the novel modulator of intestinal microbiota
Kyunghun Jeong1, Vi Nguyen2 & Jaehan Kim1,*
BMB Reports , 2012,
Abstract: Human milk, which nourishes the early infants, is a source ofbioactive components for the infant growth, development andcommensal formulation as well. Human milk oligosaccharide is agroup of complex and diverse glycans that is apparently notabsorbed in human gastrointestinal tract. Although mostmammalian milk contains oligosaccharides, oligosaccharides inhuman milk exhibit unique features in terms of their types,amounts, sizes, and functionalities. In addition to the preventionof infectious bacteria and the development of early immunesystem, human milk oligosaccharides are able to facilitate thehealthy intestinal microbiota. Bifidobacterial intestinal microbiotaappears to be established by the unilateral interaction betweenmilk oligosaccharides, human intestinal activity and commensals.Digestibility, membrane transportation and catabolic activity bybacteria and intestinal epithelial cells, all of which are linked tothe structural of human milk oligosaccharides, are crucial indetermining intestinal microbiota.
IFNγ-mediated inhibition of cell proliferation through increased PKCδ-induced overexpression of EC-SOD
Yoon-Jae Jeon1, Hyun Yoo1, Byung Hak Kim1, Yun Sang Lee1, Byeongwook Jeon1, Sung-Sub Kim2,* & Tae-Yoon Kim1,*
BMB Reports , 2012,
Abstract: Extracellular superoxide dismutase (EC-SOD) overexpressionmodulates cellular responses such as tumor cell suppression andis induced by IFNγ. Therefore, we examined the role of EC-SODin IFNγ-mediated tumor cell suppression. We observed that thedominant-negative protein kinase C delta (PKCδ) suppressesIFNγ-induced EC-SOD expression in both keratinocytes andmelanoma cells. Our results also showed that PKCδ-induced ECSODexpression was reduced by pretreatment with a PKCspecificinhibitor or a siRNA against PKCδ. PKCδ-induced ECSODexpression suppressed cell proliferations by the up-regulationof p21 and Rb, and the downregulation of cyclin A and D.Finally, we demonstrated that increased expression of EC-SODdrastically suppressed lung melanoma proliferation in an EC-SODtransgenic mouse via p21 expression. In summary, our findingssuggest that IFNγ-induced EC-SOD expression occurs via activationof PKCδ. Therefore, the upregulation of EC-SOD may beeffective for prevention of various cancers, including melanoma,via cell cycle arrest.
AMP-activated protein kinase: implications on ischemic diseases
Yong-Joo Ahn1,#, Hwewon Kim1,#, Heejin Lim2, Max Lee1, Yuhyun Kang1, SangJun Moon2, Hyeon Soo Kim3 & Hyung-Hwan Kim1,*
BMB Reports , 2012,
Abstract: Ischemia is a blockage of blood supply due to an embolism ora hemorrhage in a blood vessel. When an organ cannot receiveoxygenated blood and can therefore no longer replenish itsblood supply due to ischemia, stresses, such as the disruptionof blood glucose homeostasis, hypoglycemia and hypoxia,activate the AMPK complex. LKB1 and CaMKKβ are essentialactivators of the AMPK signaling pathway. AMPK triggersproangiogenic effects through the eNOS protein in tissues withischemic conditions, where cells are vulnerable to apoptosis,autophagy and necrosis. The AMPK complex acts to restoreblood glucose levels and ATP levels back to homeostasis. Thisreview will discuss AMPK, as well as its key activators (LKB1and CaMKKβ), as a central energy regulator and evaluate theupstream and downstream regulating pathways of AMPK. Wewill also discuss how we can control this important enzyme inischemic conditions to prevent harmful effects in patients withvascular damage.
A Study on the Genetic Inheritance of Ankyloglossia Based on Pedigree Analysis
Soo-Hyung Han,Min-Cheol Kim1,Yun-Seok Choi,Jin-Soo Lim
Archives of Plastic Surgery , 2012, DOI: http://dx.doi.org/10.5999/aps.2012.39.4.329
Abstract: Background Ankyloglossia or tongue-tie is a congenital anomaly characterized by an abnormallyshort lingual frenum. Its prevalence in the newborn population is approximately 4%. Its modeof inheritance has been studied in some articles, but no conclusion has been established. Also,no relevant report has been published in Korea. This study was conducted to elucidate thegenetic inheritance of ankyloglossia via pedigree analysis.Methods In this study, 149 patients with no other congenital anomaly who underwentfrenuloplasty between March 2001 and March 2010 were studied. Pedigrees were made viapre- or post-operative history taking, and patients with uncertain histories were excluded.In the patient group that showed a hereditary nature, the male-to-female ratio, inheritancerate, and pattern of inheritance were investigated.Results One hundred (67.11%) of the patients were male and 49 (32.89%) were female(male-female ratio=2.04:1). Ninety-one (61.07%) patients reported no other relative withankyloglossia, and 58 (38.93%) patients had a relative with this disease. The inheritance ratewas 20.69% in the 58 cases with a hereditary nature. In the group with no family history ofankyloglossia, the male-female ratio was 3.79:1, which significantly differed from that ofthe group with a family history of ankyloglossia. X-chromosome mediated inheritance andvariation in the gene expression was revealed in the pedigree drawn for the groups withhereditary ankyloglossia.Conclusions Ankyloglossia has a significant hereditary nature. Our data suggest X-linkedinheritance. This study with 149 patients, the first in Korea, showed X-linked inheritance inpatients with a sole anomaly.
Angioleiomyoma of the Auricle
Hyo-In Kim1,Si-Gyun Roh1,Nae-Ho Lee1,Kyung-Moo Yang1
Archives of Plastic Surgery , 2013, DOI: http://dx.doi.org/10.5999/aps.2013.40.1.68
Arabidopsis SIZ1 positively regulates alternative respiratory bypass pathways
Bong Soo Park1, Sung-Il Kim1, Jong Tae Song2 & Hak Soo Seo1,3,*
BMB Reports , 2012,
Abstract: Plant mitochondria possess alternative respiratory pathwaysmediated by the type II NAD(P)H dehydrogenases and alternativeoxidases. Here, E3 SUMO ligase was shown to regulatealternative respiratory pathways and to participate in the maintenanceof carbon and nitrogen balance in Arabidopsis. Thetranscript abundance of the type II NAD(P)H dehydrogenasesNDA2 and NDB2 and alternative oxidases AOX1a and AOX1dgenes was low in siz1-2 mutants compared to that in wild-type.The addition of nitrate or ammonium resulted in a decrease oran increase in the expression of the same gene families, respectively,in both wild-type and siz1-2 mutants. The amountof free sugar (glucose, fructose and sucrose) was lower in siz1-2mutants than that in wild-type. These results indicate that lownitrate reductase activity due to the AtSIZ1 mutation is correlatedwith an overall decrease in alternative respiration andwith a low carbohydrate content to maintain the carbon to nitrogenratio in siz1-2 mutants.
Inhibition of glutamate dehydrogenase and insulin secretion by KHG26377 does not involve ADP-ribosylation by SIRT4 or deacetylation by SIRT3
Eun-A Kim1,#, Seung-Ju Yang2,#, Soo Young Choi3, Woo Je Lee4,* & Sung-Woo Cho1,*
BMB Reports , 2012,
Abstract: We investigated the mechanisms involved in KHG26377 regulationof glutamate dehydrogenase (GDH) activity, focusing onthe roles of SIRT4 and SIRT3. Intraperitoneal injection of micewith KHG26377 reduced GDH activity with concomitant repressionof glucose-induced insulin secretion. Consistent withtheir known functions, SIRT4 ribosylated GDH and reduced itsactivity, and SIRT3 deacetylated GDH, increasing its activity.However, KHG26377 did not affect SIRT4-mediated ADP-ribosylation/inhibition or SIRT3-mediated deacetylation/activationof GDH. KHG26377 had no effect on SIRT4 protein levels,and did not alter total GDH, acetylated GDH, or SIRT3 proteinlevels in pancreatic mitochondrial lysates. These results suggestthat the mechanism by which KHG26377 inhibits GDHactivity and insulin secretion does not involve ADP-ribosylationof GDH by SIRT4 or deacetylation of GDH by SIRT3.
Effect of Optimized Treatment of Donor Cells on the Efficiency of Production of SCNT-Cloned Mastiffs
Sun Woo Park1,2, Yeon Woo Jeong1, Joung Joo Kim1, Kyeong Hee Ko1, Se Heon Jeong1,2, Yeon Ik Jeong1, Hye Young Son1, Mohammad Shamim Hossein1, Yeun Wook Kim1, Sang Hwan Hyun1,2*, Taeyoung Shin1 and Woo Suk Hwang1
Pakistan Veterinary Journal , 2012,
Abstract: Somatic cell nuclear transfer (SCNT) is an alternative potential tool for the conservation of endangered. In this study, somatic cells were collected from a purebred 9-month-old male mastiff and an 11-month-old female mastiff. Oocytes that had been matured in vivo were retrieved from outbred dogs by laparoscopy. We used cycling cells as donor cells for SCNT. A total of 289 oocytes were reconstructed with each male or female somatic cell and then fused/activated simultaneously by electrical stimulation. Finally, 224 embryos were transferred to 16 recipients that had been synchronized naturally. The efficiency of delivery of cloned dogs (7.1%) was threefold higher than in previous reports. Moreover, one surrogate delivered four identical cloned female Tibetan Mastiff puppies; another three surrogates each delivered triplets. Microsatellite analysis demonstrated the genotypic identity of the cloned puppies. Thus, our study has demonstrated techniques that improve significantly the overall efficiency of SCNT in the canine species.
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