• Title/Summary/Keyword: c-jun

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Taxol-Induced Apoptosis and Nuclear Translocation of Mitogen-Activated Protein (MAP) Kinase in HeLa Cells

  • Kim, Sung-Su;Kim, Yoon-Suk;Jung, Yon-Woo;Choi, Hyun-Il;Shim, Moon-Jeong;Kim, Tae-Ue
    • BMB Reports
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    • v.32 no.4
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    • pp.379-384
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    • 1999
  • Taxol, a natural product with significant anti-tumor activity, stabilizes microtubules and arrests cells in the G2/M phase of the cell cycle. It has been reported that taxol has additional effects on the cell such as an increase in tyrosine phosphorylation of proteins and activation of mitogen-activated protein (MAP) kinase. This phosphorylated kinase translocates into the nucleus and phosphorylates its substrate c-jun, c-fos, ATF2, and ATF3. The MAP kinase family is comprised of key regulatory proteins that control the cellular response to both proliferation and stress signals. First examination was cytotoxicity and apoptosis-induced concentration with paclitaxel in HeLa cell. A half-maximal inhibition of cell proliferation ($IC_{50}$) occurred at 13 nM paclitaxel. When DNA fragmentation was analyzed by agarose gel electrophoresis, a nucleosomal ladder became evident 24 h after a taxol (50 nM) addition to the cells. In addition, an apoptotic body was detected by electron microscopy. Taxol-treated cells were arrested at the S phase at 10 nM. Treatment of 50 nM taxol activated the extracellular signal-regulated protein kinase (ERK1), and a fraction of the activated MAP kinases entered the nucleus. It was also discovered that nucleus substrates c-jun was phosphorylated and activated in the cell. The activated ERK1 could subsequently translocate into the nucleus and phosphorylate its substrate c-jun as well. This study suggests that taxol-induced apoptosis might be related with signal transduction via MAP kinases.

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Characterization of the cellular localization of C4orf34 as a novel endoplasmic reticulum resident protein

  • Jun, Mi-Hee;Jun, Young-Wu;Kim, Kun-Hyung;Lee, Jin-A;Jang, Deok-Jin
    • BMB Reports
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    • v.47 no.10
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    • pp.563-568
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    • 2014
  • Human genome projects have enabled whole genome mapping and improved our understanding of the genes in humans. However, many unknown genes remain to be functionally characterized. In this study, we characterized human chromosome 4 open reading frame 34 gene (hC4orf34). hC4orf34 was highly conserved from invertebrate to mammalian cells and ubiquitously expressed in the organs of mice, including the heart and brain. Interestingly, hC4orf34 is a novel ER-resident, type I transmembrane protein. Mutant analysis showed that the transmembrane domain (TMD) of hC4orf34 was involved in ER retention. Overall, our results indicate that hC4orf34 is an ER-resident type I transmembrane protein, and might play a role in ER functions including $Ca^{2+}$ homeostasis and ER stress.

Binding Model of Fisetin and Human c-Jun NH2-Terminal Kinase 1 and Its Anti-inflammatory Activity

  • Jnawali, Hum Nath;Lee, Eunjung;Jeong, Ki-Woong;Heo, Yong-Seok;Kim, Yangmee
    • Bulletin of the Korean Chemical Society
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    • v.34 no.9
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    • pp.2629-2634
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    • 2013
  • Fisetin is a naturally occurring flavonoid with some anti-cancer and anti-inflammation capabilities. In this study, we perform docking studies between human c-Jun N-terminal kinase 1 (JNK 1) and fisetin and proposed a binding model of fisetin and JNK 1, in which the hydroxyl groups of the B ring and oxygen at the 4-position of the C ring play key roles in binding interactions with JNK. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that fisetin exhibits good binding affinity to JNK, $1.32{\times}10^8M^{-1}$. The anti-inflammatory activity of fisetin was also investigated. Fisetin significantly suppressed tumor necrosis factor, the NO production, and macrophage inflammatory cytokine release in LPS-stimulated RAW264.7 mouse macrophages. We found that the anti-inflammatory cascade of fisetin was mediated through the JNK, and cyclooxygenase (COX)-2 pathways. Our findings suggest the potential of fisetin as an anti-inflammatory agent.

Deposition condition of YBCO films by continuous source supplying MOCVD method (연속 연료공급식 MOCVD법으로 증착시킨 YBCO 박막의 증착조건)

  • Kim Ho-Jin;Joo Jin-ho;Choi Jun-Kyu;Jun Byung-Hyuk;Kim Chan-Joong
    • Progress in Superconductivity and Cryogenics
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    • v.6 no.3
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    • pp.6-11
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    • 2004
  • YBa$_2$Cu$_3$$O_{7-x}$ (YBCO) films were deposited on MgO(100) and SrTiO$_3$(100) single crystal substrates by cold-wall type MOCVD method using continuous source supplying system. Under the deposition temperature of 740∼76$0^{\circ}C$, c-axis oriented YBCO films were obtained. In case of the YBCO films deposited on MgO (100) single crystal substrate, the critical temperature (T$_{c}$) was under 81 K regardless of the deposition conditions, whereas T$_{c}$ of the YBCO films deposited on SrTiO$_3$(100) single crystal substrate was 83∼84 K. The critical current (I$_{c}$) of the YBCO film deposited on SrTiO$_3$(100) single crystal substrate for 30 min was 49 A/cm-width and the critical current density (J$_{c}$) was 0.82 MA/$\textrm{cm}^2$ to film thickness of 0.6 ${\mu}{\textrm}{m}$. I$_{c}$ increased to 84.4 A/cm-width as the deposition time increased to 50 min, but J$_{c}$ decreased to 0.53 MA/$\textrm{cm}^2$ to film thickness of 1.8 ${\mu}{\textrm}{m}$.rm}{m}$.

Induction of Apoptosis by Ursolic Acid in F9 Teratocarcinoma Cells (F9 기형암종세포에서 Ursolic acid의 apoptosis 유도기작)

  • 강창모;백진현;김규원
    • Journal of Life Science
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    • v.8 no.1
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    • pp.51-59
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    • 1998
  • The apoptosis-inducing activity of ursolic acid (UA) was examined in mouse F9 teratocarcinoma cells on the bases of biochemical and morphological characteeristics. UA, pentacyclic trierpene acid, exhibits antitumor activities including inhibition of skin tumorigenesis, induction of tumor cell differentiation and antitumor promotion. Treatment with UA showed that the decrease of cell viability was dose-dependent. UA also induced genomic DNA fragmetation, a hallmark of apoptosis, indicating that the mechanism of UA-induced F9 cell death was through apoptosis. When the morphology of the F9 cells was examined by electron microscopy, the cells treated with UA showed the charcteristic morphological features of apoptosis such as chromatin condensation and nuclear fragmentation. DNA fragmentations by UA were inhibired by cycloheximide, which suggest that de novo protein synthesis was required for DNA fragmentation by UA. Inaddition, the expression of c-jun was increased, but those of c-myc and laminin B1 were decreased during apoptosis induced by UA in F9 cells. These results suggest that UA causes an apoptosis in F9 cells. Further, the increased expression of c-jun may be involved in the UA-induced apoptosis of f9 cells.

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Effect of Heating Rates on Microstructures in Brazing Joints of STS304 Compact Heat Exchanger using MBF 20 (MBF 20으로 브레이징한 STS304 콤팩트 열교환기 접합부의 미세조직에 미치는 가열속도의 영향)

  • Kim, Jun-Tae;Heo, Hoe-jun;Kim, Hyeon-Jun;Kang, Chung-Yun
    • Journal of Welding and Joining
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    • v.34 no.2
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    • pp.46-53
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    • 2016
  • Effect of heating rate on microstructure of brazed joints with STS 304 Printed Circuit Heat Exchanger (PCHE),which was manufactured as large-scale($1170(L){\times}520(W)){\times}100(T)$, mm), have been studied to compare bonding phenomenon. The specimens using MBF 20 was bonded at $1080^{\circ}C$ for 1hr with $0.38^{\circ}C/min$ and $20^{\circ}C/min$ heating rate, respectively. In case of a heating rate of $20^{\circ}C/min$, overflow of filler metal was observed at the edge of a brazed joints showing the height of filler metal was decreased from $100{\mu}m$ to $68{\mu}m$. At the center of the joints, CrB and high Ni contents of ${\gamma}$-Ni was existed. For the joints brazed at a heating rate of $0.38^{\circ}C/min$, the height of filler was decreased from $100{\mu}m$ to $86{\mu}m$ showing the overflow of filler was not appeared. At the center of the joints, only ${\gamma}$-Ni was detected gradating the Ni contents from center. This phenomenon was driven from a diffusion amount of Boron in filler metal. With a fast heating rate $20^{\circ}C/min$, diffusion amount of B was so small that liquid state of filler metal and base metal were reacted. But, for a slow heating rate $0.38^{\circ}C/min$, solid state of filler metal due to low diffusion amount of B reacted with base metal as a solid diffusion bonding.

Involvement of Crosstalk Between cAMP and cGMP in Synaptic Plasticity in the Substantia Gelatinosa Neurons

  • Kim, Tae-Hyung;Chung, Ge-Hoon;Park, Seok-Beom;Chey, Won-Young;Jun, Sung-Jun;Kim, Joong-Soo;Oh, Seog-Bae
    • International Journal of Oral Biology
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    • v.36 no.2
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    • pp.83-89
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    • 2011
  • Substantia gelatinosa (SG) neurons receive synaptic inputs from primary afferent $A{\delta}$- and C-fibers, where nociceptive information is integrated and modulated by numerous neurotransmitters or neuromodulators. A number of studies were dedicated to the molecular mechanism underlying the modulation of excitability or synaptic plasticity in SG neurons and revealed that second messengers, such as cAMP and cGMP, play an important role. Recently, cAMP and cGMP were shown to downregulate each other in heart muscle cells. However, involvement of the crosstalk between cAMP and cGMP in neurons is yet to be addressed. Therefore, we investigated whether interaction between cAMP and cGMP modulates synaptic plasticity in SG neurons using slice patchclamp recording from rats. Synaptic activity was measured by excitatory post-synaptic currents (EPSCs) elicited by stimulation onto dorsal root entry zone. Application of 1 mM of 8-bromoadenosine 3,5-cyclic monophosphate (8-Br-cAMP) or 8-bromoguanosine 3,5-cyclic monophosphate (8-Br-cGMP) for 15 minutes increased EPSCs, which were maintained for 30 minutes. However, simultaneous application of 8-BrcAMP and 8-Br-cGMP failed to increase EPSCs, which suggested antagonistic cross-talk between two second messengers. Application of 3-isobutyl-1-methylxanthine (IBMX) that prevents degradation of cAMP and cGMP by blocking phosphodiesterase (PDE) increased EPSCs. Co-application of cAMP/cGMP along with IBMX induced additional increase in EPSCs. These results suggest that second messengers, cAMP and cGMP, might contribute to development of chronic pain through the mutual regulation of the signal transduction.

Optimal Conditions for the Mycelial Growth of Coprinus comatus Strains

  • Jang, Myoung-Jun;Lee, Yun-Hae;Liu, Jun-Jie;Ju, Young-Cheol
    • Mycobiology
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    • v.37 no.2
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    • pp.103-108
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    • 2009
  • The principal objective of this study was to acquire basic data regarding the mycelial growth characteristics for the artificial cultivation of Coprinus comatus. 12 URP primers were employed to evaluate the genetic relationships of C. comatus, and the results were divided into three groups. Among six kinds of mushroom media, MYP medium was selected as the most favorable culture medium for C. comatus. The optimal temperature and pH ranges for the mycelial growth of C. comatus were $23{\sim}26^{\circ}C$ and pH 6${\sim}$8, respectively. The carbon and nitrogen sources for optimal mycelial growth were sucrose and tryptone, respectively.

Microstructure of Tool Steel Castings for Cold-Work Die Inserts (냉간금형 인서트(insert)용 주강의 미세조직)

  • Kang, Jun-Yun;Park, Jun-Young;Kim, Hoyoung;Kim, Byunghwan
    • Journal of the Korean Society for Heat Treatment
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    • v.30 no.5
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    • pp.197-206
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    • 2017
  • The microstructure of a high-carbon and high-chromium cast steel (HK700) for cold-work die inserts was analyzed by advanced scanning electron microscopy. A continuous network of primary $M_7C_3$ carbide was developed among austenitic matrix after casting. A small amount of $M_2C$ was added to the carbide network owing to the enrichment of Mo and W during the solidification. After quenching in which the austenitization was performed at $1030^{\circ}C$ and double tempering at $520^{\circ}C$, the network structure of $M_7C_3$ was preserved while most of the matrix was transformed to martensite because of additional carbide precipitation. The $M_2C$ in the as-cast microstructure was also transformed to $M_6C$ due to its instability. The continuous network of coarse carbides owing to the absence of hot-working had little influence on the hardness after quenching and tempering, whereas it resulted in severe brittleness upon flexural loading.