• Journal of Ginseng Research
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• 제35권1호
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• pp.1-11
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• 2011

Korean ginseng is a medicinally important perennial herb from the family Araliaceae. It has been cultivated for its highly valued medicinal properties for over 1,000 years in east Asian countries such as China, Korea, and Japan. Due to its longtime cultivation in shady areas, ginseng is frequently exposed to pathogenic infections. Plants protect themselves from microbial pathogens using an array of defense mechanisms, some of which are constitutively active, while others are activated upon pathogen invasion. These induced defense responses, controlled by defense-related genes, require tradeoffs in terms of plant fitness. We hypothesize that ginseng, as with other plants, possesses regulatory mechanisms that coordinate the activation of attacker-specific defenses in order to minimize fitness costs while attaining optimal resistance. Several classes of defense-related genes are induced by infection, wounds, irradiation, and other abiotic stresses. Both salicylates and jasmonates have been shown to cause such responses, although their specific roles and interactions in signaling and development are not fully understood in ginseng. This review summarizes possible defense-related genes in ginseng based on their expression patterns against biotic and abiotic stresses and describes their functional roles.

• 미생물학회지
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• 제54권1호
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• pp.1-8
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• 2018

원핵 세포는 핵양체 결합 단백질(NAP)로 알려진 다양한 히스톤 유사 단백질을 가지고 있다. 이들은 DNA의 AT-rich 서열에 결합하여, DNA 자체를 감싸거나, 구부리거나, 떨어져 있는 DNA 가닥을 연결시키는 다리 역할을 하여, 결국에는 원핵 생물의 유전자 발현을 조절한다. NAP는 특히 전사의 억제 기능을 가지고 있기 때문에, 유전자 발현 억제에 있어서 이들의 역할과, 구체적인 메커니즘을 밝히는 것을 매우 중요한 일이다. 본 논문에서는 잘 알려져 있는 NAP인 H-NS와 HU에 대하여 정리하였고, 특히 E. coli와 Salmonella Typhimurium에서 이들의 유전자 발현에 대한 기능을 요약하였다. H-NS는 이들의 올리고머화와 필라멘트 구조 형성을 통하여 Salmonella와 같은 사람에 감염하는 병원성 세균의 독성유전자 발현을 억제할 수 있고, 이런 기능을 수행하였을 때 다른 NAP와 함께 작용할 수 있다. 최근에 H-NS는 사람에게 typhoid fever와 systemic disease를 발생시키는 독성물질인, typhoid toxin의 발현 또한 조절할 수 있음이 밝혀졌다. Salmonella에서 HU 또한 독성 유전자뿐만 아니라, 이들의 생리적 기능에 중요한 유전자들의 발현을 조절할 수 있다. 따라서, H-NS와 HU와 같은 NAP들이 원핵 생물의 독성 유전자 발현의 분자적인 메커니즘을 밝히는데 중요한 요소임을 제시한다.

• Journal of Medicine and Life Science
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• 제18권3호
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• pp.41-48
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• 2021

The prevalence of attention deficit hyperactivity disorder (ADHD), a developmental neuropsychiatric disorder, is high among children and adolescents. The pathogenesis of ADHD is mediated with genetic, biological, and environmental factors. Most therapeutic drugs for ADHD have so far targeted biological causes, primarily by regulating catecholaminergic neurotransmitters. However, ADHD drugs that are clinically treated have various problems in their addictiveness and drug stability; thus, it is recommended that efficacy and safety should be secured through simultaneous prescription of multiple drugs rather than a single drug treatment. Accordingly, it is necessary to develop drugs that newly target pathogenic mechanisms of ADHD. In this study, we attempt to confirm the possibility of developing new drugs by reviewing dopamine-related developmental mechanisms of neurons and their correlation with ADHD. Histone deacetylase inhibitors (HDACi) can regulate the concentration of intracellular dopamine in neurons by expressing vesicular monoamine transporter 2 and inducing the exocytosis of neurotransmitters to the synaptic cleft, thereby promoting the development of neurons and signal transmission. This cellular modulation of HDACi is expected to treat ADHD by regulating endogenous catecholamines such as dopamine. Although studies are still in the preclinical stage, HDAC inhibitors clearly have potential as a therapeutic agent with low addictiveness and high efficacy for ADHD treatment.

• Annals of Clinical Neurophysiology
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• 제10권2호
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• pp.98-100
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• 2008

Restless legs syndrome (RLS) is a sensorimotor neurological disorder in which the primary symptom is a compelling urge to move the legs, accompanied by unpleasant and disturbing sensations in the legs. Although pathophysiologic mechanism of RLS is still unclear, several evidences suggest that RLS is related to dysfunction in central nervous system involving brain and spinal cord. L-DOPA, as the precursor of dopamine, as well as dopamine agonists, plays an essential role in the treatment of RLS leading to the assumption of a key role of dopamine function in the pathophysiology of RLS. Patients with RLS have lower levels of dopamine in the substantia nigra and respond to iron administration. Iron, as a cofactor in dopamine production, plays a central role in the etiology of RLS. Functional neuroimaging studies using PET and SPECT support a central striatal D2 receptor abnormality in the pathophysiology of RLS. Functional MRI suggested a central generator of periodic limb movements during sleep (PLMs) in RLS. However, to date, we have no direct evidence of pathogenic mechanisms of RLS.

• Genomics & Informatics
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• 제13권1호
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• pp.2-6
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• 2015

Pathogenic bacteria survive in iron-limited host environments by using several iron acquisition mechanisms. Acinetobacter baumannii, causing serious infections in compromised patients, produces an iron-chelating molecule, called acinetobactin, which is composed of equimolar quantities of 2,3-dihydroxybenzoic acid (DHBA), L-threonine, and N-hydroxyhistamine, to compete with host cells for iron. Genes that are involved in the production and transport of acinetobactin are clustered within the genome of A. baumannii. A recent study showed that entA, located outside of the acinetobactin gene cluster, plays important roles in the biosynthesis of the acinetobactin precursor DHBA and in bacterial pathogenesis. Therefore, understanding the genes that are associated with the biosynthesis and transport of acinetobactin in the bacterial genome is required. This review is intended to provide a general overview of the genes in the genome of A. baumannii that are required for acinetobactin biosynthesis and transport.

• 대한수의학회지
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• 제52권4호
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• pp.259-262
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• 2012

Classical swine fever (CSF) is a highly contagious disease among swine that has an important economic impact on worldwide. One clinical symptom of CSF is leukopenia, in particular lymphopenia, which is a characteristic event that occurs early in the course of CSF. Though lymphopenia associated with apoptosis, the pathogenic mechanism underlying the lymphopenia has not been well studied. To understand these mechanisms, we investigated the response of porcine B cell lines to infection with SW03, virulent strain isolated from swine tissue in Korea. This study demonstrated that SW03-infected L35 cell were induced apoptosis through the detection of activated caspase-3. In addition, SW03 infection leaded to alterations in pro-apoptotic, Bax, and anti-apoptotic, Bcl-xL proteins of Bcl-2 family. Our results would suggest that SW03-infected L35 cells induced apoptosis via intrinsic mitochondrial pathway.

• Journal of Microbiology and Biotechnology
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• 제28권2호
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• pp.181-189
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• 2018

Candida albicans is a major pathogenic fungus in humans, and meets at first the innate immune cells, such as macrophages, in its host. One important strategy of the host cell to kill C. albicans is to produce reactive oxygen species (ROS) by the macrophages. In response to ROS produced by the macrophages, C. albicans operates its defense mechanisms against them by expressing its oxidative stress response genes. Although there have been many research studies explaining the specific transcription factors and the expression of the oxidative stress genes in C. albicans, the regulation of the oxidative stress genes by chromatin structure is little known. Epigenetic regulation by the chromatin structure is very important for the regulation of eukaryotic gene expression, including the chromatin structure dynamics by histone modifications. Among various histone modifications, histone acetylation is reported for its direct relationship to the regulation of gene expression. Recent studies reported that histone acetyltransferases regulate genes to respond to the oxidative stress in C. albicans. In this review, we introduce all histone acetyltransferases that C. albicans contains and some papers that explain how histone acetyltransferases participate in the oxidative stress response in C. albicans.

• Asian Pacific Journal of Cancer Prevention
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• 제15권22호
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• pp.9853-9857
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• 2014

Background: The morbidity and mortality rate of liver cancer continues to rise in China and advanced cases respond poorly to chemotherapy. Ribosomal protein L24 has been reported to be a potential therapeutic target whose depletion or acetylation inhibits polysome assembly and cell growth of cancer. Materials and Methods: Total RNA of cultured amycin-resistant and susceptible HepG2 cells was isolated, and real time quantitative RT-PCR were used to indicate differences between amycin-resistant and susceptible strains of HepG2 cells. Viability assays were used to determine amycin resistance in RPL24 transfected and control vector and null-transfected HepG2 cell lines. Results: The ribosomal protein L24 transcription level was 7.7 times higher in the drug-resistant HepG2 cells as compared to susceptible cells on quantitative RT-PCR analysis. This was associated with enhanced drug resistance as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions: The ribosomal protein L24 gene may have effects on drug resistance mechanisms in hepatocellular carcinoma HepG2 cells.

• 한국미생물·생명공학회지
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• 제34권4호
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• pp.289-298
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• 2006

3',5'-cyclic adenosine monophosphate (cAMP) is an important molecule, which mediates diverse cellular processes. For example, it is involved in regulation of sugar uptake/catabolism, DNA replication, cell division, and motility in various acterial species. In addition, cAMP is one of the critical regulators for syntheses of virulence factors in many pathogenic bacteria. It is believed that cAMP acts as a signal for environmental changes as well as a regulatory factor for gene expressions. Therefore, intracellular concentration of cAMP is finely modulated by according to its rates of synthesis (by adenylate cyclase), excretion, and degradation (by cAMP phosphodiesterase). In the present review, we discuss the bacterial physiological characteristics governed by CAMP and the molecular mechanisms for gene regulation by cAMP. Furthermore, the effect of cAMP on phosphotransferase system is addressed.

• 대한의생명과학회지
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• 제19권3호
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• pp.173-179
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• 2013

Since the identification and characterization of toll-like receptors (TLR) in Drosophila, numerous scientific studies have examined the role of TLRs in host innate immunity. Recent studies have suggested a convergence of the nuclear factor kappa B (NF-${\kappa}B$) signaling and cytokine production regulated by the cytosolic elicitor known as NLRs (nucleotide-binding domain and leucine-rich repeat containing domain receptors) as a key modulator in inflammatory diseases. Among the NLRs, NOD1 and NOD2 have been intensively investigated for its role in inflammatory bowel disease (IBD). On the other hand, NLRs such as NLRP3, NLRP1, and NLRC4 (also known as IPAF) have been identified to form the inflammasome to activate downstream signaling molecules in response to pathogenic microbes. There is evidence to suggest that substantial crosstalk exists for the TLR and NLR signaling pathway in response to pathogen associated molecular pattern (PAMP). However, the substrate and the mechanistic role of NLRs are largely unknown in innate immune response. Understanding the signaling mechanisms by which NLRs recognize PAMP and other danger signals will shed light on elucidating the pathogenesis of various human inflammatory diseases such as IBD.