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하주헌(Joohun Ha) 한국창조과학회 2022 Origin Research Journal Vol.2 No.2
생물학에서 돌연변이는 DNA의 염기서열의 변화를 의미한다. 현대 분자생물학을 통해 잘 확립된 유전 정보의 발현 순서는 DNA로부터 RNA가 만들어지고 RNA로부터 단백질이 만들어진다는 것이다. 유전 정보를 갖는 DNA로부터 실질적 기능을 수행하는 단백질이 만들어지는 일련의 과정을 센트럴 도그마라고 부른다. 따라서 DNA에 일어나는 돌연변이는 생명체에 막대한 영향을 유발할 수 있다. 이러한 돌연변이는 세포가 복제되는 과정에서 자연스럽게 발생할 뿐 아니라 다양한 세포 내외부의 자극에 의해 발생하기도 한다. 사람의 경우, 이러한 돌연변이가 발생할 때, 원래의 염기 서열로 복원시키는 다양한 DNA 복구 시스템이 존재한다. 본 논문에서는 암 발생 과정과 진화 과정에서 추정되는 돌연변이의 역할을 비교해 보고자 한다. In biology, mutation indicates alterations in the sequence of nucleic acid of an organism. The most-well established flow of expression of genetic information is that RNA is made from DNA and the protein is made from RNA. This process is called central dogma. Therefore, mutations in DNA can significantly affects various aspects of the organisms. DNA mutations occur naturally during the cell division, and it can be caused by extra or intracellular stresses. Humans have a variety of DNA repair system, which identifies mutations or DNA damages and repair them. In the present study, I will compare and analyze the putative role of mutation during tumorigenesis and evolution process.
Costunolide Triggers Apoptosis in Human Leukemia U937 Cells by Depleting Intracellular Thiols
Choi, Jung-Hye,Ha, Joohun,Park, Jae-Hoon,Lee, Jae Yeol,Lee, Yong Sup,Park, Hee-Juhn,Choi, Jong-Won,Masuda, Yutaka,Nakaya, Kazuyasu,Lee, Kyung-Tae WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 2002 東西醫學硏究所 論文集 Vol.2002 No.-
We have preciously demonstrated that costunolide, a biologically active compound that was isolated from the stem bark of Magnolia sieboldii, induced apoptosis in human cancer cells. In the present study, we investigated the underlying mechanisms and suggest that costunlide induces apoptosis in human promonocytic leukemia U937 cells by depleting the intracellular thiols. Cos-tunolide treatment rapidly depleted the intracellular reduced glutathione (GSH) and protein thiols, and this prereded the ocrurrence of apoptosis. Pretreatment with sulfhydryl compounds such as GSH, N-acetyl-L-cysteline, dithiothreitol and 2-mercaptoethanol almost completely blocked the costunolide-induced apoptosis, highlighting the significance of the intracellular thiol level in the Process. Furthermore, overexpression or Bcl-2 also significantly attenuated the effects of costunolide.The apoptosis-inducing activity of costunolide is likely to depend on the exomethylene moiety because derivatives in which this group was reduced, such as dihydrocostunolide and saussurea lactone, did not deplete the cellular thiols and showed no apoptotic activity. Taken together, the present study demonstrates that the costunolide-induced apoptosis depends on intracellu1ar thiols contents, which are modulated by Bcl-2.
Seo, Bo-Rim,Lee, Kyung-Won,Ha, Joohun,Park, Hee-Jun,Choi, Jong-Won,Lee, Kyung-Tae WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 2004 東西醫學硏究所 論文集 Vol.2004 No.-
In the present study, we investigated the in vitro effect of saucernetin-7, which is a dineolignan isolated from Saururus chinensis, on the proliferation, cell cycle-regulation and differentiation of HL-60 human promyelocytic leukemia cells. Saucernetin-7 potently inhibited the proliferation of HL-60 cells in both a dose- and time-dependent manner with an IC_(50), ~5 μM. DNA flow-cytometry indicated that saucernetin-7 markedly induced a G₁ phase arrest of HL-60 cells. Among the G₁ phase cell cyclerelated proteins, the levels of cyclin-dependent kinase (CDK)6 and cyclin D1 were reduced by saucernetin-7, whereas the steady-state levels of CDK2, CDK4, cyclin D2, cyclin D3 and cyclin E were unaffected. The protein and mRNA levels of a CDK inhibitor p21^(CIP1/WAF1), but not p27^(KIP1), were markedly increased by saucernetin-7 and p21^(CIP1/WAF1) induction is likely to occur at the transcriptional level because actinomycin D blocked this induction. In addition, saucernetin-7 markedly enhanced the binding of p21^(CIP1/WAF1) with CDK2 and CDK6, resulting in the reduced activity of both kinases and the hypophosphorylation of Rb protein. We furthermore suggest that saucernetin-7 is a potent inducer of the differentiation of HL-60 cells, based on observations such as a reduction of the nitroblue tetrazolium level, an increase in the esterase activities and phagocytic activity, morphology changes, and the expression of CD14 and CD66b surface antigens. In conclusion, the onset of saucernetin-7-induced the G_(0)/G₁ arrest of HL-60 cells prior to the differentiation is Iinked to a sharp up-regulation of the p21^(CIP1/WAF1) level and a decrease in the CDK2 and CDK6 activities. This is the first report demonstrating that saucernetin-7 potently inhibits the proliferation of human promyelocytic HL-60 cells via the G₁ phase cell cycle arrest and differentiation induction.
Induction of Apoptosis by Yomogin in Human Promyelocytic Leukemic HL-60 Cells
JEONG, Seoung-Hee,KOO, Sung-Ja,HA, Joo-Hun,RYU, Shi-Yong,PARK, Hee-Juhn,LEE, Kyung-Tae WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 2004 東西醫學硏究所 論文集 Vol.2004 No.-
Yomogin is an active compound isolated from Artemisia princep, a traditional Oriental medicinal herb, which has been shown to inhibit tumor cell proliferation. In this study, we investigated the effects of yomogin on the cytotoxicity, induction of apoptosis, and putative pathways of its actions in human promyelocytic leukemia cells. Yomogin-treated HL-60 cells displayed several features of apoptosis, including DNA fragmentation, formation of DNA ladders in agarose gel electrophoresis, and externalization of annexin-V targeted phosphatidylserine residues. We observed that yomogin caused activation of caspase-8, caspase-9, and caspase-3. A general caspase inhibitor (z-VAD-fmk), caspase-8 inhibitor (z-IETD-fmk) and caspase-3 inhibitor (z-DEVD-fmk), almost completely suppressed the yomogin-induced DNA fragmentation. We further demonstrated that yomogin induced Bid cleavage, mitochondrial translocation of Bax from the cytosol, and cytochrome c release from mitochondria in a caspase-8-dependent manner. Taken together, our data indicate that yomogin is a potent inducer of apoptosis and facilitates its activity via caspase-8 activation, Bid cleavage, Bax translocation to mitochondria, and subsequent release of cytochrome c into the cytoplasm, providing a potential mechanism for the anticancer activity of yomogin.
Neuroprotective Effects of AMP-Activated Protein Kinase on Scopolamine Induced Memory Impairment
김수정,이준호,정환석,송주현,하주헌,배현수 대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, is activated in response to cellular stress when intracellular levels of AMP increase. We investigated the neuroprotective effects of AMPK against scopolamine-induced memory impairment in vivo and glutamate-induced cytotoxicity in vitro. An adenovirus expressing AMPK wild type alpha subunit (WT) or a dominant negative form (DN) was injected into the hippocampus of rats using a stereotaxic apparatus. The AMPK WT-injected rats showed significant reversal of the scopolamine induced cognitive deficit as evaluated by escape latency in the Morris water maze. In addition, they showed enhanced acetylcholinesterase (AChE)-reactive neurons in the hippocampus, implying increased cholinergic activity in response to AMPK. We also studied the cellular mechanism by which AMPK protects against glutamateinduced cell death in primary cultured rat hippocampal neurons. We further demonstrated that AMPK WT-infected cells increased cell viability and reduced Annexin V positive hippocampal neurons. Western blot analysis indicated that AMPK WT-infected cells reduced the expression of Bax and had no effects on Bcl-2, which resulted in a decreased Bax/Bcl-2 ratio. These data suggest that AMPK is a useful cognitive impairment treatment target, and that its beneficial effects are mediated via the protective capacity of hippocampal neurons.
Park, Hee-Juhn,Kim, Ryung-Gue,Seo, Bo-Rim,Ha, Joohun,Ahn, Byung-Tae,Bok, Song-Hae,Lee, Yong Sup,Kim, Hyoung Ja,Lee, Kyung-Tae WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 2003 東西醫學硏究所 論文集 Vol.2003 No.-
In the present study, we demonstrate that saucernetin-8(1) and saucernetin-7 (2), isolated from the underground parts of Sauiurus chinensis (Saururaceae), exerted potent inhibitory effects on LPS-induced nitric oxide (NO) and prostaglandin E_(2)(PGE_(2)) production in RAW 264.7 cells. Both compounds 1 and 2, known as dineolignans, also suppressed the expression of iNOS and COX-2 protein in a dose-dependent manner. Thus, this study suggests that compounds 1 and 2-mediated inhibition of iNOS and COX-2 expression may be one of the mechanisms responsible for the anti-inflammatory effects of the underground parts of Saururus chinensis.
KIM, Rung-Gyu,SHIN, Kyung-Min,KIM, Young-Kwan,JEONG, Hyeh-Jean,HA, Joohun,CHOI, Jong-Won,PARK, Hee-Juhn,LEE, Kyung-Tae WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 2003 東西醫學硏究所 論文集 Vol.2003 No.-
As an attempt to search for bioactive natural products exerting antunflammatory activity, we have evaluated the effects of the methanol extract from the aerial parts of Saururus chinensis (LouR.) BaILL (Saururaceae) on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E_(2)(PCE_(2)) release by the macrophage cell line RAW 264.7. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased PGE_(2) release. Consistent with these observations, the protein and mRNA expression level of inducible NO synthase ((1)_NOS) and cyclooxyagenase (COX)-2 was inhibited by MeOH extracts of the aerial part of S chinensis (SCM) in a dose-dependent manner. Furthermore, SCM inhibited the LPS-induced DNA binding activity of nuclear factor-kB (NF-kB), which was associated with decreased p65 protein levels in the nucleus. These results suggest that SCM inhibits LPS-induced (1)_NOS and COX-2 expression by blocking NF-kB activation.