• 제목/요약/키워드: cytochrome C

검색결과 1,177건 처리시간 0.029초

Oxidation of Dibenzothiophene Catalyzed by Surfactant-Hemoprotein Complexes in Anhydrous Nonpolar Organic Solvents

  • Ryu, Keun-Garp;Chae, Young-Rae;Kwon, O-Yul
    • Journal of Microbiology and Biotechnology
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    • 제13권5호
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    • pp.647-650
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    • 2003
  • In anhydrous organic solvents, the complexes formed between AOT (dodecylbenzene sulfuric acid sodium salt) and hemoproteins, such as hemoglobin, myoglobin, or cytochrome c, displayed remarkably higher activity than the hemoprotein powders to oxidize dibenzothiophene, a model compound of organic sulfurs contained in fossil fuels. In slightly hydrophobic organic solvents, such as ethyl acetate and butyl acetate, dibenzothiophene was completely oxidized catalytically by the cytochrome c-AOT complex with cumene hydroperoxide (${\alpha},{\alpha}-dimethylbenzyl$ hydroperoxide) as an oxidant. In highly hydrophobic organic solvents, such as decane and hexadecane, however, the activity of the cytochrome c-AOT complex decreased, presumably due to the aggregation of the hemoprotein-AOT complex in these solvents.

Potentiation of Ceramide-Induced Apoptosis by $p27^{kip1}$ Overexpression

  • Kim Hae Jong;Ghil Kyung Chul;Kim Moo Sung;Yeo Seong Hyun;Chun Young Jin;Kim Mie Young
    • Archives of Pharmacal Research
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    • 제28권1호
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    • pp.87-92
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    • 2005
  • The cyclin-dependent kinase inhibitor$p27^{kip1}$(p27) has been implicated in the regulation of cell cycle and apoptosis. Recently, we have demonstrated that ceramide induces apoptotic cell death associated with increase in the level of p27 in HL-60 cells. In the present study, we showed that overexpression of p27 increases ceramide-induced apoptotic cell death in HL-60 cells. Furthermore, overexpression of p27 accelerated DNA fragmentation, PARP cleavage and cytochrome c release induced by ceramide. In addition, ceramide induced Sax expression independent of p27. These findings indicate that enhanced effect on apoptosis by p27 is associated with mitochondrial signaling which involves cytochrome c release.

Stock Characterization of the Fleshy Prawn (Penaeus chinensis) in the Yellow Sea by Intraspecific Sequence Variation of the Cytochrome c Oxidase Subunit I Gene

  • HWANG Gyu-Lin
    • 한국수산과학회지
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    • 제29권6호
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    • pp.876-881
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    • 1996
  • To determine the amount of genetic variation among populations of Penaeus chinensis (Osbeck) in the Yellow Sea, 342 bp region of the mitochondrial cytochrome c oxidase subunit I gene was amplified and sequenced. Six haplotypes, which differ by from one to four nucleotide sustitutions, were detected from 34 individuals of 4 populations examined. Mean sequence divergence between pairs of haplotypes was $0.68\%$. Most individuals from 4 populations were shared by the most common genotype. This genotype was distributed evenly in the Korean and Chinese populations. This result is in accordance with findings observed using RFLPs analysis of mtDNA (Hwang et al., 1997). Therefore, it is suggested that P. chinensis should be treated as one unit stock in the Yellow Sea.

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Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation

  • Seo, Hong Joo;Choi, Sang Joon;Lee, Jung-Hee
    • Biomolecules & Therapeutics
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    • 제22권6호
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    • pp.503-509
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    • 2014
  • Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells.

Effect of Alcohol Addition on Back-Extraction of BSA and Cytochrome c Using AOT Reverse Micellar System

  • 이성식;이봉국;최진성;이종팔
    • Bulletin of the Korean Chemical Society
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    • 제22권8호
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    • pp.897-902
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    • 2001
  • The protein back-extraction processes were discussed from the viewpoint of the micelle-micelle interaction. Bovine serum albumin (BSA) suppressing the cluster formation of reverse micelle (positive value of ${\beta}pr)$ has the high back-extra cted fraction (Eb), but cytochrome c enhancing the formation of reverse micelle (negative value of ${\beta}pr)$ has the low back-extracted fraction, relatively. We have also examined quantitatively the effects of alcohol addition and protein solubilization on the percolation process of reverse micelle. The alcohols suppressing the formation of micellar cluster (high values of ${\beta}t)$, remarkably improved the back-extraction rates of BSA and cytochrome c. The values of ${\beta}t$, defined by the variation of percolation process, and the back-extraction behavior of proteins have a good linear correlation. These results indicate that the micelle-micelle interaction or micellar clustering plays an important role in the back-extraction process of proteins.

Paramagnetic Inversion of the Sign of the Interference Contribution to the Transverse Relaxation of the Imido Protons of the Coordinated Imidazoles in the Uniformly $^{15}N$ Labeled Cytochrome $c_3$

  • ;정인철;심윤보;강신원;박장수
    • Bulletin of the Korean Chemical Society
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    • 제22권11호
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    • pp.1197-1201
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    • 2001
  • In the spectrum of uniformly 15N labeled cytochrome c3, the relative linewidths of the doublet peaks of the 15N-coupled imido proton of the coordinated imidazole group were reversed on oxidation. This inversion was explained by the interference relaxation process between the electron-proton dipolar and 15N-1H dipolear interactions. The inversion can be used to assign the imido protons of the coordinated imidazole groups in heme proteins.

Up-regulation of Cyelin A-Cdk2 activity is associated with depolarization of mitochondrial membrane potential during apoptosis of human hepatoma SK-HEP1 cells induced by treatment with panaxadiol

  • Park, Byoung-Duck;Jin, Ying-Hua;Yim, Hyung-Shin;Lee, Seung-Ki
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.167.1-167.1
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    • 2003
  • Here we show that panaxadiol, a ginseng saponin with a dammarane skeleton, induces acute apoptotic cell death in human hepatoma SK-HEP-1 cells as evidenced by analysis of DNA fragmentation, caspase activation, and changes in cell morphology. The kinetic study showed that panaxadiol-induced apoptosis is associated with depolarization of mitochondrial membrane potential and cytochrome c release. Sequential activations of caspases-depolarization of mitochondrial membrane potential and cytochrome c release. Sequential activations of caspases-9, and -3, or -7, but not of caspase 8 coincide well in a time dependent manner with mitochondrial membrane depolarization and cytochrome c release from mitochondria during apoptosis of SK-HEP-1 cells induced by treatment with panaxadiol. (omitted)

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Induction of apoptosis in human promyelocytic leukaemia HL -60 cells by yomogin involves release of cytochrome c and activation of caspase

  • Jeong, Seoung-Hee;Koo, Sung-Ja;Ryu, Shi-Yong;Park, Hee-Jun;Lee, Kyung-Tae
    • 대한약학회:학술대회논문집
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    • 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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    • pp.319.1-319.1
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    • 2002
  • Yomogin. an eudesmane sesquiterpene isolated from Artemisia princeps, was found to induce apoptosis in human promyelocytic leukaemia, HL -60 cell with characteristic apoptotic features like nuclear condensation, apoptotic body formation, flipping of membrane phosphatidylserine, release of mitochondrial cytochrome c and caspase-8. -9. and -3 activation. Furthermore. early yomogin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAd fmk and preceded loss of mitochondrial membrane potential. The results suggest that induction of apoptosis by yomogin may provide a pivotal mechanism for their cancer chemopreventive function.

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Tributyltin Induces Apoptosis in R2C via Oxidative Stress and Caspase-3 Activation by Disturbance of $Ca^{2+}$

  • Lee, Kyung-Jin;Lee, Jong-Bin
    • 환경생물
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    • 제21권3호
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    • pp.303-307
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    • 2003
  • Tributyltin (TBT) used world-wide in antifouling paints toy ships is a wide-spread environmental pollutant. At low doses, antiproliferative modes of action have been shown to be involved, whereas at higher doses apoptosis seems to be the mechanism of toxicity in reproductive organs by TBT. In this study, we investigated that the mechanisms underlying apoptosis induced by TBT in R2C cell. Effects of TBT on intracellular $Ca^{2+}$ level and reactive oxygen species (ROS) were investigated in R2C cells by fluorescence detector. TBT significantly induced intracellular $Ca^{2+}$ level in a time-dependent manner. The rise in intracellular $Ca^{2+}$ level was followed by a time-dependent generation of reactive oxygen species (ROS) at the cytosol level. Simultaneously, TBT induced the release of cytochrome c from the mitochondrial membrane into the cytosol. Furthermore, ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular $Ca^{2+}$ chelator, indicating the important role of $Ca^{2+}$ in R2C during these early intracellular events. In addition, Z-DEVD FMB, a caspase -3 inhibitor, decreased apoptosis by TBT. Taken together, the present results indicated that the apoptotic pathway by TBT might start with an increase in intracellular $Ca^{2+}$ level, continues with release of ROS and cytochrome c from mitochondria, activation of caspases, and finally results in DNA fragmentation.

Gonadotropin Releasing Hormone-Agonist가 임신된 흰쥐 황체세포의 세포자연사에 미치는 영향 (Effect of Gonadotropin Releasing Hormone-Agonist on Apoptosis of Luteal Cells in Pregnant Rat)

  • 양현원;김종석;박철홍;윤용달
    • 한국발생생물학회지:발생과생식
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    • 제6권2호
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    • pp.131-139
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    • 2002
  • 최근 난포에서 GnRH와 그 수용체의 발현이 확인되면서 GnRH가 국소적으로 난소의 기능을 조절하고,특 히 과립세포의 세포자연사(apoptosis)를 유도하는 것으로 보고되고 있다. 그러나 황체에서 GnRH와 그 수용체의 발현과 기능에 대해서는 잘 알려져 있지 않다. 따라서 본 연구는 임신한 흰쥐의 황체세포에서 GnRH와 그 수용체가 발현되는지를 확인하고, 또한 GnRH가 황체세포의 세포자연사를 직접적으로 유발시킬 수 있는지를 알아보고자 시행하였다. 임신된 흰쥐로부터 황체세포를 획득하여 배양한 후 면역조직화학적 염색과 Western blot 방법으로 GnRH와 그 수용체의 발현을 확인한 결과 배양된 황체세포에서 GnRH와 그 수용체가 강하게 발현되는 것을 관찰할 수 있었다. GnRH가 배양된 황체세포의 세포자연사에 미치는 영향을 조사하기 위하여, $10^{-6}$ GnRH-agonist(GnRH-Ag)를 처리한 후 3, 8, 12시간에 TUNEL 방법과 DNA 분절화 검증 방법으로 세포자연사를 조사하였다. TUNEL 결과 세포자연사를 보이는 황체세포는 처리 후 12 시간에 GnRH-Ag 처리군에서 유의하게 증가하였다(p<0.05). 또한 DNA 분절화를 조사한 결과에서도 TUNEL 결과와 유사하게 GnRH-Ag처리 후 12 시간에 DNA 분절화가 유의하게 증가하였다(p<0.05). 이러한 세포자연사의 증가가 cytochrome c 방출과 연관이 있는지를 알아보고자 미토콘드리아로부터 방출된 cytochrome c를 Western blot 방법으로 정량한 결과, GnRH-Ag 처리 후 12 시간에 cytochrome c가 미토콘드리아로부터 세포질쪽으로 방출된 것을 확인할 수 있었다. 결론적으로 임신된 흰쥐의 황체세포에서 GnRH와 그 수용체 단백질이 발현되며 GnRH-Ag가 GnRH 수용체에 결합함으로써 cytochrome c가 미토콘드리아로부터 방출되고, 이로 인해 황체세포가 세포자연사하는 것을 알 수 있었다. 이러한 결과들은 국소적으로 분비되는 GnRH가 미토콘드리아로부터 cytochrome c의 방출을 유발시켜 황체세포의 세포자연사를 유도할 수 있다는 것을 제시하고 있다.

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