1,843,131 research outputs found
Kwon Hyuk-Kwon
No full text학위논문(박사)--아주대학교 일반대학원 :분자과학기술학과,2015. 2Contents
ACKNOWLEDGMENTS
ABSTRACT
Chapter 1. Etoposide Induces Necrosis through P53-mediated Antiapoptosis 1
1.1 Abstract 1
1.2 Introduction 2
1.3 Results. 4
ETO Induced DNA Damage Response (DDR) Proteins, Formation of γ-H2AX Foci, and a Cell Cycle Arrest. 4
ETO Induced Oxidative Stress and Mitochondrial Biogenesis. 5
Inhibition of P53 Abrogated a Cell Cycle Arrest and Induction of DDR Proteins; These Events Enhanced ETO-induced DNA Damage and Cytotoxicity. 6
Inhibition of P53 Affected Mitochondrial Biogenesis, Oxidative Stress and Caspase 3 Activation. 6
Inhibition of P53 Induced Cell Adhesion Disruption and Apoptosis. 7
Inhibition of P53 Induced a Morphological Transition from Necrosis to Apoptosis. 8
A P53 Knockdown Reduced the cROS Generation and Induced Caspase 3 and Apoptosis. 9
1.4 Discussion 10
1.5 Methods 14
1.6 Figure and Figure legends 20
1.7 Supplements Figure and Supplements Figure legends. 33
1.8 References 41
Chapter 2. New Label-free Measurement Methods for The Analysis of Nuclear Envelope Topography and Cell Adhesion in Necrosis and Apoptosis 46
2.1 Abstract 46
2.2 Introduction 47
2.3 Results. 49
DOX Completely Induced Necrosis, while ETO Induced Necrosis in Combination with Apoptosis 49
Necrosis and Nepoptosis Generated Cell Swelling, but Yield Different Effects on Cell Adhesion 49
Preservation of Necrotic Morphological Changes during Necrosis and Nepoptosis 50
Necrosis and Nepoptosis Generated Nucleus Swelling and Altered Nucleus Morphology 51
Nepoptosis Induced NE Rupturing and DNA Leakage from The Nuclei 52
Cell Adhesion Disruption and NE Rupturing Are Induced by Caspase Activation during Nepoptosis. 52
ENDOG Is Translocated in The Nucleus through Caspase-induced NE Rupturing during Nepoptosis. 53
2.4 Discussion 54
2.5 Methods 57
2.6 Figure and Figure legends 63
2.7 Supplements Figure and Supplements Figure legends 71
2.8 References 78
Chapter 3. APPENDIX 81
1. Paper 1: ATF3 Plays a Key Role in Kdo2-Lipid A-Induced TLR4-Dependent Gene Expression via NF-kB Activation 81
2. Paper 2: Capric Acid Inhibits NO Production and STAT3 Activation during LPS-Induced Osteoclastogenesis 91
3. Paper 3: Doxorubicin Induces Cytotoxicity through Upregulation of pERKDependent ATF3 100
4. Paper 4: Discovery of an Integrative Network of MicroRNAs and Transcriptomics Changes for Acute Kidney Injury 111
Chapter 4. 국문요약 123DoctoralEven though various chemotherapeutic drugs are being used for clinical trials, until now, the field of scientific research keeps on carrying several studies aiming the development of relatively safe and stable anti-cancer drugs. Unfortunately, the continued use of the chemotherapeutic drug has the major limitation of severe side-effects in various organs. In particular, in case of p53, which is a key transcription factor known for its important role in the modulation of multiple cellular signaling pathways. The mutation occurring in p53 gene has been reported to be the cause of 75% of cancer’s cases suggesting that the loss of p53 function might lead to tumorigenesis. However, the exact mechanism by which the p53 causes cell death by DNA damage through apoptosis or necrosis, is not yet fully understood. Moreover, a clear understanding of the various modifications occurring in both cell adhesion and nuclear envelope features related to cell death remains largely unknown. To address this subject, our present study investigated the observed modifications in cell adhesion ability and nuclear envelope changes as well as DNA damage caused by p53 regulated apoptosis and necrosis, by using the Topoisomerase II targeting chemotherapeutic drugs such as etoposide and/or doxorubicin. For this, a variety of bio/nano-technological methods were used during.
The first results of this study showed that the treatment of the human renal proximal tubule derived cells (HK-2) by etoposide induced DNA damage, p53 activation, cell cycle arrest and triggered the generation of reactive oxygen species (ROS) as well the mitochondrial biogenesis. Moreover, cell morphological changes such as cell swelling and plasma membrane rupture were also confirmed by carbon nanotube atomic force microscopy (CNT/AFM) analysis. In the other hand, the treatment of the p53-defective cells by etoposide limited cell cycle arrest and the mitochondrial biogenesis while it induced the increase of DNA damage, ROS mitochondrial generation and nitric oxide (NO) synthesis. Moreover, mitochondria outer membrane protein degradation as well as caspase 3 activation also increased. The morphological changes such cell shrinkage and the formation of apoptotic body were confirmed by the use of the CNT/AFM analysis. These findings show that the p53 activation, through the DNA damage signals, is responsible for the inhibition of cell death by apoptosis and the activation of necrosis.
The second result of this study showed that though the treatment of the HK-2 cell by etoposide and doxorubicin induced the change of morphological features into those noticed in necrosis, in the case of cells treated by etoposide both apoptosis and necrosis features were observed while in the case of doxorubicin only necrosis morphological characteristic were reported. Based on the above experimental conditions, the morphological changes of cell during the mechanism of cell death by apoptosis were measured in real time by the xCELLigene: cells size, cell adhesion area and cell adhesion speed were formulated based on that adhesive properties of the cells were confirmed. The results showed that in apoptosis the cells presented a decrease in cell adhesion area as well as a decrease in their speed of adhesion. In the other hand in case of necrosis the speed of cell adhesion didn't present any significant change while an increase in the cell adhesion area was reported. In addition, in both cases of apoptosis and necrosis the changes of the nuclear envelope were investigated using CNT/AFM analysis and the result of the investigation showed that in necrotic cells the nuclear envelope did not present any damage. The nuclear pore complex as well as the general form of the nuclear envelope was confirmed. However, in case of apoptosis the rupture of the nuclear envelope as well as the nuclear pore destruction due to the activated caspase were also showed.
Moreover, in the present work, DNA fragmentation protein translocation in nucleus through the rupture of the nuclear envelope caused by caspase, were also detected.
In the present study, even though apoptosis and necrosis features such as changes in cell adhesion properties and changes in the nuclear envelope features were characterized, new methods of measurement using the nano-technology will be recommended in order to overcome the limitations of conventional measurement methods.
In conclusion, through the fusion of various bio- and nano-chemical technologies we studied cell death, used a variety of methods that helped to understand cell death mechanisms
Scaphomonus naejangsanus Dutta & Kwon & Suh & Kwon 2020, sp. nov.
No full textScaphomonus naejangsanus sp. nov. Distribution. Korea.Published as part of Dutta, Nirmal Kumar, Kwon, Jin Hyung, Suh, Sang Jae & Kwon, Yong Jung, 2020, First record of the leafhopper genus Scaphomonus Viraktamath from Korea, with description of one new species (Hemiptera: Cicadellidae: Deltocephalinae), pp. 191-195 in Zootaxa 4747 (1) on page 192, DOI: 10.11646/zootaxa.4747.1.9, http://zenodo.org/record/369353
Interview with Sylvia Kwon
No full textSylvia Kwon has been living in California for 20 years but she grew up in the Midwest. Her parents are first generation Korean immigrants. She started sewing for her son\u27s ballet studio and ever since then found interest in sewing, she’s very creative and learned how to sew on her own and started with very little basic things. Sylvia Kwon is very centered around her community; she not only helped sew costumes for her son\u27s ballet studio but has also sent around face masks that she’s made. She’s made over 1000 face masks as well as sewn a quilt for a school fundraiser.https://digitalcommons.csumb.edu/auntiesewing_interviews/1011/thumbnail.jp
Ji-Woong Kwon
No full text학위논문(석사)--아주대학교 일반대학원 :분자과학기술학과,2014. 8Acknowledgement.............................................................................................ⅰ
Abstract............................................................................................................ ⅱ
List of Figures.................................................................................................. ⅵ
Introduction.........................................................................................................1
Results..................................................................................................................4
LPS-induced inflammatory responses in Raw 264.7 Cells..............................4
ATF3 direct binds and regulates p65................................................................4
ATF3 inhibits LPS-induced nucleus translocation of NF-κB..........................5
Activation of NF-κB by ATF3 regulation........................................................6
ATF3 regulates NF-κB dependent gene expression.........................................8
Discussion...........................................................................................................21
Materials and Methods.....................................................................................24
Cell culture....................................................................................................24
RNA isolation and RT (Reverse Transcription) – PCR..................................24
Western blot analysis.....................................................................................25
Immunoprecipitation (IP) analysis................................................................26
IL-6 secretion analysis...................................................................................26
P65 Enzyme-linked immunosorbent assay (ELISA).....................................27
SEAP reporter assay......................................................................................27
NO (Nitric Oxide) assay................................................................................28
siRNA design and transfection......................................................................28
References..........................................................................................................30
국문요약.............................................................................................................35MasterATF3 is a transcription factor that encodes a CREB / ATF family member and well known about stress inducible gene. ATF3 is induced under inflammatory responses or cell death, cytokines and oxidative stress condition. LPS-induced ATF3 is a role as negative regulator which represses generation of cytokine such as NO, IL-6, IL-12β and TNF-α in TLR4 signaling pathway. In this signaling, the key molecule which emerges inflammatory response is NF-κB. It is kwon that if p65, subunit of NF-κB, is translocated to nucleus, cytokines such as NO, IL-6, IL-12β and TNF-α are expressed. However, it has not been discovered interaction between p65 and ATF3. So we found directly interaction p65 and ATF3 using LPS-induced Raw 264.7 cell. First, we confirmed expression of NF-κB signaling after LPS treatment, and then observed that ATF3 and p65 were bound directly. In ATF3 deficient cells, NF-kB activity was up-regulated so we could guess ATF3 negative regulates p65 via binding with p65 and HDAC1. Likewise, we observed that inflammatory response genes which were induced by NF-κB activation were up-regulated in ATF3 deficient cells than control. In this result, we discovered that ATF3 plays as a negative regulator that inhibits activity of NF-κB via directly interaction with p65 subunit of NF-κB. ATF3 could bind promoter in the target cytokine genes and recruit with HDAC1 (Histone Deacetylase 1) so they deacetylased κB site in the promoter. But in this study, we discovered that ATF3 doesn’t inhibit target genes only, but also regulates NF-κB via binding to p65. Our results suggest that this is another regulation mechanism of ATF3 for negative regulator in TLR4 signaling pathway
Bactericera sarahae Kwon & Kwon 2020
No full textBactericera sarahae Kwon & Kwon, 2020 Bactericera (Klimaszewskiella) sarahae Kwon & Kwon, 2020: 214. Distribution in Korea. GB (Kwon & Kwon 2020, as Bactericera (Klimaszewskiella) sarahae). Host plant. Adults were collected on Salix L. (Salicaceae) (Kwon & Kwon 2020) which needs to be confirmed as host.Published as part of Cho, Geonho, Burckhardt, Daniel & Lee, Seunghwan, 2022, Check list of jumping plant-lice (Hemiptera: Psylloidea) of the Korean Peninsula, pp. 1-91 in Zootaxa 5177 (1) on page 66, DOI: 10.11646/zootaxa.5177.1.1, http://zenodo.org/record/702193
Cacopsylla kimae Kwon & Kwon 2020
No full textCacopsylla kimae Kwon & Kwon, 2020 Cacopsylla (Hepatopsylla) kimae Kwon & Kwon, 2020: 159. Distribution in Korea. JJ, JN (Kwon & Kwon 2020, as Cacopsylla (Hepatopsylla) kimae). Host plant. Elaeagnus macrophylla Thunb. (Elaeagnaceae) (Kwon & Kwon 2020).Published as part of Cho, Geonho, Burckhardt, Daniel & Lee, Seunghwan, 2022, Check list of jumping plant-lice (Hemiptera: Psylloidea) of the Korean Peninsula, pp. 1-91 in Zootaxa 5177 (1) on page 47, DOI: 10.11646/zootaxa.5177.1.1, http://zenodo.org/record/702193
Cacopsylla yunae Kwon & Kwon 2020
No full textCacopsylla yunae Kwon & Kwon, 2020 Cacopsylla (Hepatopsylla) yunae Kwon & Kwon, 2020: 186. Distribution in Korea. GB, GW (Kwon & Kwon 2020, as Cacopsylla (Hepatopsylla) yunae). Host plant. Adults were collected on Malus baccata (L.) Borkh. (Rosaceae) (Kwon & Kwon 2020) which needs to be confirmed as host.Published as part of Cho, Geonho, Burckhardt, Daniel & Lee, Seunghwan, 2022, Check list of jumping plant-lice (Hemiptera: Psylloidea) of the Korean Peninsula, pp. 1-91 in Zootaxa 5177 (1) on page 60, DOI: 10.11646/zootaxa.5177.1.1, http://zenodo.org/record/702193
Cacopsylla longiventris Kwon & Kwon 2020
No full textCacopsylla longiventris Kwon & Kwon, 2020 Cacopsylla (Hepatopsylla) longiventris Kwon & Kwon, 2020: 163. Distribution in Korea. GW (Kwon & Kwon 2020, as Cacopsylla (Hepatopsylla) longiventris). Host plant. Salix L. (Salicaceae) (Kwon & Kwon 2020). Comments. According to Kwon & Kwon (2020), C. longiventris is close to C. arcuata Loginova, 1965, reported from Kazakhstan, Mongolia and Russia (Primorsky Krai, Siberia) (Labina 2008), but differs in the more reduced surface spinules of the forewings. If this difference justifies species status should be examined with additional material.Published as part of Cho, Geonho, Burckhardt, Daniel & Lee, Seunghwan, 2022, Check list of jumping plant-lice (Hemiptera: Psylloidea) of the Korean Peninsula, pp. 1-91 in Zootaxa 5177 (1) on page 49, DOI: 10.11646/zootaxa.5177.1.1, http://zenodo.org/record/702193
Colophorina flaveola Kwon & Kwon 2020
No full textColophorina flaveola Kwon & Kwon, 2020 (Fig. 56) Colophorina flavivittata sensu Cho, Burckhardt & Lee 2017a: 537, nec Li 1992a: 144. Colophorina flaveola Kwon & Kwon, 2020: 95. Distribution in Korea. GB, GG, GN (Cho et al. 2017a, as Colophorina flavivittata; Kwon & Kwon 2020) (KNA, NHMB, NIBR, SNU). Host plant. Gleditsia sinensis Lam. (Fabaceae) (Cho et al. 2017a); Kwon & Kwon (2020) reported Gleditsia japonica Miq. as host based on the findings of adults. Comments. According to the original description, C. flaveola is morphologically close to C. flavivittata (Li 1992a) from which it differs in the shape of the genal processes. If these differences reflect inter- or intraspecific variation needs further studies. Meanwhile we regard C. flaveola as a valid species.Published as part of Cho, Geonho, Burckhardt, Daniel & Lee, Seunghwan, 2022, Check list of jumping plant-lice (Hemiptera: Psylloidea) of the Korean Peninsula, pp. 1-91 in Zootaxa 5177 (1) on page 33, DOI: 10.11646/zootaxa.5177.1.1, http://zenodo.org/record/702193
Erythroneura (Ziczacella) Hossain & Kwon & Suh & Kwon 2019
No full textGenus. Ziczacella Anufriev, 1970 Ziczacella Anufriev, 1970, Bull. Acad. Pol. Sci. (Ser. Sci. Biol.) 17(11, 12): 697. Type species. Erythroneura heptapotamica Kusnezov, 1928 Type locality. Middle Asia Description. Body moderately slender, head narrower than pronotum. General coloration yellowish, often with pair of dark spots on crown, or sometimes lacking; brown pattern on pronotum and scutellum; zigzagged stripe on forewing. Crown angulate medially, moderately produced, broadly rounded apically. Head including eyes narrower than pronotum. Second sternal apodeme in male with posterior lobes generally not well developed. Male genitalia. Pygofer lobe rounded or subangularly produced, not reaching apex of subgenital plate posteriorly; dorsal processes movably articulated, rather long, well sclerotized, running along the inner side of pygofer lobe posteriorly. Subgenital plate gently curved upwards and rounded apically in lateral view, with 2¯4 basal macrosetae. Style narrowed apically, with two slender apical and one short triangular subapical processes; inner apical process slender, apparently longer than outer one. Connective with stem absent or very short, depressed, without median anterior lobe; arms long. Aedeagus with shaft usually articulated with pair of robust pincer-shaped processes basally, rarely with shaft firmly fused to base with processes arising from base; shaft with or without processes distally.Published as part of Hossain, Md. Shamim, Kwon, Jin Hyung, Suh, Sang Jae & Kwon, Yong Jung, 2019, Taxonomic revision of the microleafhopper genus Ziczacella Anufriev 1970 from Korea (Hemiptera: Cicadellidae: Typhlocybinae), pp. 363-372 in Zootaxa 4571 (3) on pages 363-364, DOI: 10.11646/zootaxa.4571.3.4, http://zenodo.org/record/261273
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