• 한국식품조리과학회지
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• 제13권5호
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• pp.661-668
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• 1997

By using several solvents, barley extracts containing the anticomplementary activities in classical pathway were prepared (250 $\mu\textrm{g}$/ml): methanol (83.1%), ethanol (71.9%), water extract (25.4%), M-1 (250 $\mu\textrm{g}$/ml), and the soluble part of methanol extract which showed the highest activity (83.4%) and the yield. Anticomplementary activity of methanol extract as well as protease digestion in classical pathway showed 82.4% and 78.4% in the concentration of 250 $\mu\textrm{g}$/ml, respectively. It was found that protein was not involved in anticomplementary activity in the classical pathway and the methanol extract made an impact on classical pathway, but not on alternative pathway. For the immune-stimulating effect, the T cell proliferation effect of the protease digestion displayed little effect irrespective of the dose. In addition, the T cell proliferation effect of methanol extract showed 13-fold higher proliferation effect compared with positive control. It was revealed that the substance containing protein serves as an important factor for the immune proliferation. Therefore, the anticomplementary activity ${\beta}$-glucan in classical pathway and alternative pathway displayed the lowest activity, showing 2.2%, 22.3% respectively. However, the immune-stimulating effect of ${\beta}$-glucan showed the T cell stimulating effect 13 times higher than positive control.

• 한국식품영양학회지
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• 제9권4호
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• pp.490-495
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• 1996

홑파래로부터 황산기를 함유한 다당체를 크로마토그래프로 분리정제하여 rhamnan sulfate가 항보체 활성화에 미치는 영향을 조사하였다. 항보체 활성능력은 F-4-3 획분을 비교군으로 Heparin H-180, Dextran과 비교해 결과 비교군보다 높았고, C4a와 C3a의 C convertase의 형성과 기능을 F-4-3 획분이 억제하였다. 이러한 보체 활성화 양식은 classical pathway 및 alternative pathway로도 경유함을 알 수 있었다.

• Natural Product Sciences
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• 제14권3호
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• pp.196-201
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• 2008

Five neolignans (1 - 4, 8), two sesquiterpene-lignans (5 - 6), and two phenylpropanoids (7, 9) were isolated from the stem bark of Magnolia obovata Thunberg (Magnoliaceae) by repeated column chromatography. The structures of isolated compounds were identified as 4-methoxyhonokiol (1), obovatol (2), magnolol (3), honokiol (4), eudeshonokiol B (5), eudesobovatol B (6), coumaric acid (7), magnaldehyde B (8), and ${\rho}-coumaric$ acid (9) on the basis of spectroscopic analysis including 2D-NMR and MS data. Compounds 1 - 9 were evaluated for their anti-complement activities against the classical pathway of the complement system. Of them, compound 8 showed significant anti-complement activity on the classical pathway with $IC_{50}$ value of 102.7 ${\mu}M$, whereas compounds 1 - 7 and 9 were inactive. This result indicated that an aldehyde group in the neolignan is important for the anti-complement activity against the classical pathway.

• Journal of Veterinary Science
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• 제22권3호
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• pp.36.1-36.12
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• 2021

Background: Mouse hepatitis virus (MHV) A59 is a highly infectious pathogen and starts in the respiratory tract and progresses to systemic infection in laboratory mice. The complement system is an important part of the host immune response to viral infection. It is not clear the role of the classical complement pathway in MHV infection. Objectives: The purpose of this study was to determine the importance of the classical pathway in coronavirus pathogenesis by comparing C1qa KO mice and wild-type mice. Methods: We generated a C1qa KO mouse using CRISPR/Cas9 technology and compared the susceptibility to MHV A59 infection between C1qa KO and wild-type mice. Histopathological and immunohistochemical changes, viral loads, and chemokine expressions in both mice were measured. Results: MHV A59-infected C1qa KO mice showed severe histopathological changes, such as hepatocellular necrosis and interstitial pneumonia, compared to MHV A59-infected wild-type mice. Virus copy numbers in the olfactory bulb, liver, and lungs of C1qa KO mice were significantly higher than those of wild-type mice. The increase in viral copy numbers in C1qa KO mice was consistent with the histopathologic changes in organs. These results indicate that C1qa deficiency enhances susceptibility to MHV A59 systemic infection in mice. In addition, this enhanced susceptibility effect is associated with dramatic elevations in spleen IFN-γ, MIP-1 α, and MCP-1 in C1qa KO mice. Conclusions: These data suggest that C1qa deficiency enhances susceptibility to MHV A59 systemic infection, and activation of the classical complement pathway may be important for protecting the host against MHV A59 infection.

• 도시과학
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• 제9권2호
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• pp.45-50
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• 2020

The formation characteristics of calcium carbonates are closely related to the durability and mechanical properties of cement-based materials. In this regard, a deep understanding of the reaction pathway of calcium carbonates is critical. Recently, non-classical nucleation theory was summarized and it was presumed that prenucleation clusters are present. The formation of the prenucleation cluster at undersaturated condition (≈ 0.1 ml) in the present study was investigated via electrical characteristics of an electrolytic solution. Calcium chloride dihydrate (CaCl2·2H2O) and sodium carbonate (Na2CO3) were used as starting materials to supply calcium and carbonate sources, respectively. Furthermore, the reaction pathway of calcium carbonates was investigated by time-resolved polarization and depolarization characteristics of the electrolytic solution. The time-resolved polarization and depolarization tests were conducted by switching polarity with an interval of 20 seconds for 1 hr and by measuring the variation of electrical resistance. It can be inferred from the results obtained in the present study that the reactive constituent for the formation of calcium carbonates was mostly consumed in the period possibly associated with the prenucleation and the reaction pathways may be governed by the monomer-addition mechanism.

• Molecules and Cells
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• 제39권3호
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• pp.169-178
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• 2016

Although $N{\alpha}$-terminal acetylation (Nt-acetylation) is a pervasive protein modification in eukaryotes, its general functions in a majority of proteins are poorly understood. In 2010, it was discovered that Nt-acetylation creates a specific protein degradation signal that is targeted by a new class of the N-end rule proteolytic system, called the Ac/N-end rule pathway. Here, we review recent advances in our understanding of the mechanism and biological functions of the Ac/N-end rule pathway, and its crosstalk with the Arg/N-end rule pathway (the classical N-end rule pathway).

• 한국식품과학회지
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• 제34권2호
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• pp.290-295
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• 2002

김치 및 발효유 제품으로부터 분리한 유산균과 공시균주 12종을 대상으로 보체 용혈 분석법을 이용하여 면역계에서 중요한 역할을 담당하고 있는 보체계 활성화(항보체 활성, $TCH_{50}$) 정도를 측정한 결과, 김치로 부터 분리한 Lactobacillus plantarum이 타 유산균 종에 비해 높은 활성을 나타내었다. 이들 균주로 부터 조제된 세포벽 획분의 경우 세포질 획분보다도 높은 활성을 보였으며 각 획분의 활성은 농도 의존적 경향을 나타내었다. L. plantarum의 세포질 획분과 세포벽 획분의 경우 pronase 소화 후에는 활성의 변화가 없는 반면, 과요오드산 처리에 의해서는 급격한 활성의 감소를 나타내는데 이들 결과로부터 L. plantarum의 세포질과 세포벽 획분에 의한 보체계 활성화가 주로 다당 영역에 기인함을 알수 있었다. 한편 anti-human C3를 이용한 2차원 면역전기영동에 의해, $Ca^{++}$ 이온을 제거한 상태에서도 세포질과 세포벽 획분에 의한 C3 활성화 산물을 동정할 수 있었다. 또한 L. plantarum의 세포벽 획분에 의한 항보체 활성은 동일 조건에서 활성을 유지한 반면, 세포질 획분에 의한 활성화 정도는 동일 조건에서 상당히 감소하였다. 이상의 결과로부터 L. plantarum 세포벽 획분의 보체계 활성화 양식은 주로 alternative pathway의 활성화에 의한 것이며, 세포질 획분에 의한 활성화는 classical pathway와 alternative pathway 양 경로를 경유함을 알 수 있었다.

• Journal of Microbiology and Biotechnology
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• 제16권3호
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• pp.391-398
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• 2006

$NF-{\kappa}B$ is a transcription factor involved in the innate immunity against bacterial infection and inflammation. It is also known to render cells resistant to the apoptosis caused by some anticancer drugs. Such a chemoresistance of cancer cells may be related to the activation of $NF-{\kappa}B$ transcription factor; however, the mechanism of activation is not well understood. Here, we demonstrate that a chemotherapeutic agent, etoposide, independently stimulates the $I{\kappa}B{\alpha}$ degradation pathway and PI3-kinase/Akt signaling pathway: The classical $I{\kappa}B{\alpha}$ degradation pathway leads to the nuclear translocation and DNA binding of p65 subunit through $IKK{\beta}$ kinase, whereas the PI3-kinase/Akt pathway plays a distinct role in activating this transcription factor. The PI3-kinase/Akt pathway acts on the p50 subunit of the $NF-{\kappa}B$ transcription factor and enhances the DNA binding affinity of the p50 protein. It may also explain the role of the PI3-kinase/Akt pathway in the anti-apoptotic function of $NF-{\kappa}B$ during chemoresistance of cancer cells.

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2008년도 International Meeting of the Microbiological Society of Korea
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• pp.23-25
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• 2008

Serum complement proteins comprise an important system that is responsible for several innate and adaptive immune defence mechanisms. There were three well described pathways known to lead to the generation of a C3 convertase, which catalyses the proteolysis of complement component C3, and leads to the formation of C3 opsonins (C3b, iC3b and C3d) that fix to bacteria. A pivotal step in the complement pathway is the assembly of a C3 convertase, which digests the C3 complement component to form microbial-binding C3 fragments recognized by leukocytes. The spleen clears microorganisms from the blood. Individuals lacking this organ are more susceptible to Streptococcus pneumoniae. Innate resistance to S. pneumoniae has previously been shown to involve complement components C3 and C4, however this resistance has only a partial requirement for mediators of these three pathways, such as immunoglobulin, factor B and mannose-binding lectin. Therefore it was likely that spleen and complement system provide resistance against blood-borne S. pneumoniae infection through unknown mechanism. To better understand the mechanisms involved, we studied Specific intracellular adhesion molecule-grabbing nonintegrin (SIGN)-R1. SIGN-R1, is a C-type lectin that is expressed at high levels by spleen marginal-zone macrophages and lymph-node macrophages. SIGN-R1 has previously been shown to be the main receptor for bacterial dextrans, as well as for the capsular pneumococcal polysaccharide (CPS) of S. pneumoniae. We examined the specific role of this receptor in the activation of complement. Using a monoclonal antibody that selectively downregulates SIGN-R1 expression in vivo, we show that in response to S. pneumoniae or CPS, SIGN-R1 mediates the immediate proteolysis of C3 and fixation of C3 opsonins to S. pneumoniae or to marginal-zone macrophages that had taken up CPS. These data indicate that SIGN-R1 is largely responsible for the rapid C3 convertase formation induced by S. pneumoniae in the spleen of mice. Also, we found that SIGN-R1 directly binds C1q and that C3 fixation by SIGN-R1 requires C1q and C4 but not factor B or immunoglobulin. Traditionally C3 convertase can be formed by the classical C1q- and immunoglobulin-dependent pathway, the alternative factor-B-dependent pathway and the soluble mannose-binding lectin pathway. Furthermore Conditional SIGN-R1 knockout mice developed deficits in C3 catabolism when given S. pneumoniae or its capsular polysaccharide intravenously. There were marked reductions in proteolysis of serum C3, deposition of C3 on organisms within SIGN-$R1^+$ spleen macrophages, and formation of C3 ligands. The transmembrane lectin SIGN-R1 therefore contributes to innate resistance by an unusual C3 activation pathway. We propose that in the SIGN-R1 mediated complement activation pathway, after binding to polysaccharide, SIGN-R1 captures C1q. SIGN-R1 can then, in association with several other complement proteins including C4, lead to the formation of a C3 convertase and fixation of C3. Therefore, this new pathway for C3 fixation by SIGN-R1, which is unusual as it is a classical C1q-dependent pathway that does not require immuno globulin, contributes to innate immune resistance to certain encapsulated microorganisms.

• 동의생리병리학회지
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• 제33권4호
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• pp.191-197
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• 2019

This study aims to evaluate the effects of the root bark of Morus alba (RMA) on the regulation of the Hippo-YAP pathway. Hippo-YAP signaling is a critical regulator in controlling organ size and tissue homeostasis. Hippo, the serine/threonine kinase phosphorylate the LATS. Phosphorylated LATS then phosphorylates and inactivates the YAP and TAZ, which are two closely related transcriptional co-activator. Here we report RMA activates the Hippo signaling, thereby inhibits the YAP/TAZ activity. First, we examine the cytotoxic effects of RMA by MTT assay. RMA was cytotoxic at concentrations higher than $50{\mu}g/ml$ in HEK293A cells. The reporter gene assay was performed to measure the activity of TEAD, a key transcription factor that controls cell growth and proliferation. RMA significantly suppressed the luciferase activity. By phos-taq gel shift assay, and western blotting, we showed that RMA enhanced the phosphorylation of YAP in wild type cells, but not in LATS1/2 knock out cells, which means RMA activates classical Hippo pathway. RMA induced the cytoplasmic sequestration of YAP. RMA also suppressed the mRNA expression of CTGF and CYR61; the two major YAP dependent genes. Taken together, RMA is considered to be a good candidate for proliferative disease such as cancer, by facilitating cell death through activating the Hippo signaling pathway.