• BMB Reports
• /
• 제31권3호
• /
• pp.227-232
• /
• 1998

The leukocyte NADPH oxidase of neutrophils is a membrane-bound enzyme that catalyzes the production of $O_2^-$ from oxygen using NADPH as an electron donor. Dormant in resting neutrophils, the enzyme acquires catalytic activity when the cells are exposed to appropriate stimuli. During activation, the cytosolic oxidase components $p47^{phox}$ and $p67^{phox}$ migrate to the plasma membrane, where they associate with cytochrome $b_{558}$, a membrane-bound flavohemoprotein, to assemble the active oxidase. The oxidase can be activated in a cell-free system; the activating agent usually employed is an anionic amphiphile such as sodium dodecyl sulfate (SDS). Because $p47^{phox}$ can translocate by itself during activation, the conformational change in $p47^{phox}$ may be responsible for the activation of NADPH oxidase. We show here that the treatment of $p47^{phox}$ with SDS leads to an increase in the reactivity of the sutbydryl group of cysteines toward N-ethylmaleimide, indicating that the conformational change occurs when $p47^{phox}$ is exposed to SDS. We propose that this change in conformation results in the appearance of a binding site through which $p47^{phox}$ interacts with cytochrome $b_{558}$during the activation process.

• Carbon letters
• /
• 제4권2호
• /
• pp.57-63
• /
• 2003

In polymer precursor based activated carbon, the structure of starting material is likely to have profound effect on the surface properties of end product. To investigate this aspect phenolic resins of different types were prepared using phenol, mcresol and formaldehyde as reactants and $Et_3N$ and $NH_4OH$ as catalyst. Out of these resins two resol resins PFR1 and CFR1 (prepared in excess of formaldehyde using $Et_3N$ as catalyst in the basic pH range) were used as raw materials for the preparation of activated carbons by both chemical and physical activation methods. In chemical activation process both the resins gave activated carbons with high surface areas i.e. 2384 and 2895 $m^2/g$, but pore size distribution in PFR1 resin calculated from Horvath-Kawazoe method, contributes mainly in micropore range i.e. 84.1~88.7 volume percent of pores was covered by micropores. Whereas CFR1 resin when activated with KOH for 2h time, a considerable amount (32.8%) of mesopores was introduced in activated carbon prepared. Physical activation with $CO_2$ leads to the formation of activated carbon with a wide range of surface area (503~1119 $m^2/g$) with both of these resins. The maximum pore volume percentage was obtained in 3-20 ${\AA}$ region by physical activation method.

• Environmental Engineering Research
• /
• 제20권3호
• /
• pp.205-211
• /
• 2015

Reduced forms of iron, such as zero-valent ion (ZVI) and ferrous ion (Fe[II]), can activate dissolved oxygen in water into reactive oxidants capable of oxidative water treatment. The corrosion of ZVI (or the oxidation of (Fe[II]) forms a hydrogen peroxide ($H_2O_2$) intermediate and the subsequent Fenton reaction generates reactive oxidants such as hydroxyl radical ($^{\bullet}OH$) and ferryl ion (Fe[IV]). However, the production of reactive oxidants is limited by multiple factors that restrict the electron transfer from iron to oxygen or that lead the reaction of $H_2O_2$ to undesired pathways. Several efforts have been made to enhance the production of reactive oxidants by iron-induced oxygen activation, such as the use of iron-chelating agents, electron-shuttles, and surface modification on ZVI. This article reviews the chemistry of oxygen activation by ZVI and Fe(II) and its application in oxidative degradation of organic contaminants. Also discussed are the issues which require further investigation to better understand the chemistry and develop practical environmental technologies.

• 한국초전도학회:학술대회논문집
• /
• 한국초전도학회 1999년도 High Temperature Superconductivity Vol.IX
• /
• pp.262-265
• /
• 1999

We report the activation energies which is calculated by adding a term being neglected usually, and magnetic relaxation effects for the surface barrier. The activation energies U at initial magnetization m (m$_{en}$ and m$_{ex}$) and equilibrium magnetization m$_{eq}$ are nearly similar to those of Burlachkov, but the m dependence of the activation energy U is remarkably different. The relaxation effects, which were determined by the m dependence of the activation energies U, are nonlinear for vortex entry, but linear at the initial stage and nonlinear at m(Int) ${\simeq}$ m$_{eq}$ for vortex exit. During relaxation process, the vortex entry at m = m$_{en}$ is faster than the vortex exit at m = m$_{ex}$ by about factor 90. The vortex exit at m = m$_{eq}$ is faster than one at m = m$_{ex}$ by about factor 1.3

• BMB Reports
• /
• 제40권6호
• /
• pp.888-894
• /
• 2007

Src homology (SH) domains of phospholipase C-$\gamma1$ (PLC-$\gamma1$) impair NGF-mediated PC12 cells differentiation. However, whether the enzymatic activity is also implicated in this process remains elusive. Here, we report that the enzymatic activity of phospholipase C-$\gamma1$ (PLC-$\gamma1$) is at least partially involved to the blockage of neuronal differentiation via an abrogation of MAPK activation, as well as sustained Akt activation. By contrast, Overexpression of WT-PLC-$\gamma1$ exhibited sustained NGF-induced MAPK activation, and triggered transient Akt activation resulting in profound inhibition of neurite outgrowth. However, lipase-inactive mutant (LIM) PLC-$\gamma1$ cells fail to suppress neurite outgrowth, although it contains intact SH domains, specifically enhancing the expression of cyclin D1 and p21 proteins, which regulate the function of retinoblastoma Rb protein. These observations show that the lipase inactive mutant of PLC-$\gamma1$ does not alter NGF-induced neuronal differentiation via enzymatic inability and the modulation of cell cycle regulatory proteins independent on SH3 domain.

• Molecules and Cells
• /
• 제25권4호
• /
• pp.504-509
• /
• 2008

Three G-protein-linked acetylcholine receptors (GARs) exist in the nematode C. elegans. GAR-3 is pharmacologically most similar to mammalian muscarinic acetylcholine receptors (mAChRs). We observed that carbachol stimulated ERK1/2 activation in Chinese hamster ovary (CHO) cells stably expressing GAR-3b, the predominant alternatively spliced isoform of GAR-3. This effect was substantially reduced by the phospholipase C (PLC) inhibitor U73122 and the protein kinase C (PKC) inhibitor GF109203X, implying that PLC and PKC are involved in this process. On the other hand, GAR-3b-mediated ERK1/2 activation was inhibited by treatment with forskolin, an adenylate cyclase (AC) activator. This inhibitory effect was blocked by H89, an inhibitor of cAMP-dependent protein kinase A (PKA). These results suggest that GAR-3b-mediated ERK1/2 activation is negatively regulated by cAMP through PKA. Together our data show that GAR-3b mediates ERK1/2 activation in CHO cells and that GAR-3b can couple to both stimulatory and inhibitory pathways to modulate ERK1/2.

• 한국발생생물학회지:발생과생식
• /
• 제16권1호
• /
• pp.69-75
• /
• 2012

Hatching occurred in the time dependent manners and strictly controlled. Although, the hatching processes are under the control of muti-embryotrophic factors and the expressed G proteins of cell generate integrated activation, the knowledge which GPCRs are expressed during hatching stage embryos are very limited. In the present study, which G proteins are involved was examined during blastocyst development to the hatching stage. The early-, expanded-, and lobe-stage blastocysts were treated with various $G_{\alpha}$ activators and H series inhibitors, and examined developmental patterns. Pertusis toxin (PTX) improved the hatching rate of the early-stage blastocyst and lobe-formed embryos. Cholera toxin (CTX) suppressed the hatching of the early-stage blastocyst and expanded embryos. The effects of toxins on hatching and embryo development were changed by the H7 and H8. These results mean that PTX mediated GPCRs activation is signaling generator in the nick or pore formation in the ZP. In addition, PTX mediated GPCR activation induces the locomotion of trophectoderm for the escaping. CTX mediate GPCRs activation is the cause of suppression of hatching processes. Based on these data, it is suggested that various GPCRs are expressed in the periimplantation stage embryos and the integration of the multiple signals decoding of various signals in a spatial and temporal manner regulate the hatching process.

• 공업화학
• /
• 제4권1호
• /
• pp.113-124
• /
• 1993

Polyacrylonitrile계 섬유를 전구체로 하여 비등온 과정에 의한 활성화를 승온속도를 달리한 TGA(thermogravimetric analysis) 방법으로 연구하였다. 탄소섬유 -$H_2O$(30%)-$N_2$계 비등온 활성화 과정에서 유도된 속도식 $f=1-\exp(-a{\Delta}T)^b$는 실험값과 잘 일치하였다. 전환율에 따른 세공 용적은 pore volume model에 의한 이론값과 비교적 잘 일치하였고, 이때의 세공 구조는 승온속도, 활성화 온도와 내부 및 외부 전환율과의 복합적인 작용에 의하여 결정되었다.

• 동의생리병리학회지
• /
• 제19권2호
• /
• pp.501-507
• /
• 2005

Shikonin is a chemically characterized component of traditional herbal medicine, the root of Lithospermum erythrorhizon and has been shown to possess antitumor activities. Here we investigated anticancer potential of shikonin and its possible mechanism of action in LLC cells. Shikonin inhibited the proliferation of LLC cells in a concentration-dependent manner. It was also demonstrated that shikonin induced apoptosis in LLC cells by Annexin V staining and TUNEL staining analysis. Shikonin treatment was caused that decrease of Bcl-2, activation of caspases and cleavage of PARP. And shikonin also induced that the activation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Interestingly, the cell proliferation inhibition induced by shikonin was recovered by specific inhibitors of JNK and p38 but the inhibitor of MEK, the upstream kinase of ERK, did not recover. Additionally, shikonin administration at doses of 5 mg/kg in C57BL/6 mice strongly inhibited the primary tumor growth of LLC. Taken together, these results suggest that shikonin may suppress LLC cell proliferation by inducing an apoptotic process via activation of caspases and MAPKs

• Journal of Applied Biological Chemistry
• /
• 제64권3호
• /
• pp.317-322
• /
• 2021

Among the different cardiovascular disorders (CVDs), the activation of platelets is a necessary step. Based on this knowledge, therapeutic treatments for CVDs that target the disruption of platelet activation are proving to be worthwhile. One such substance, a bioactive 6,7-dihydroxy derived from coumarin, is 6,7-Dihydroxy-2H-1-benzopyran-2-one (esculetin). This compound has demonstrated several pharmacological effects on CVDS as well as various other disorders including diabetes, obesity, and renal failure. In various reports, esculetin and its effect has been explored in experimental mouse models, human platelet activation, esculetin-inhibited collagen, and washed human platelets exhibiting aggregation via arachidonic acid. Yet, esculetin affected aggregation with agonists like U46619 or thrombin in no way. This study investigated esculetin and how it affected human platelet aggregation activated through U46619. Ultimately, we confirmed that esculetin had an effect on the aggregation of human platelets when induced from U46619 and clarified the mechanism. Esculetin interacts with the downregulation of both phosphoinositide 3-kinase/Akt and mitogen-activated protein kinases, important phosphoproteins that are involved in activating platelets and their signaling process. The effects of esculetin reduced TXA₂ production, phospholipase A₂ activation, and platelet secretion of intracellular granules (ATP/serotonin), ultimately causing inhibition of overall platelet aggregation. These results clearly define the effect of esculetin in inhibiting platelet activity and thrombus formation in humans.