• Journal of Embryo Transfer
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• v.33 no.1
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• pp.49-54
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• 2018

Adenomyosis is a benign gynecological disease frequently affecting women of reproductive age. It has a negative impact on the quality of life, causing bleeding disorders, dysmenorrhea, chronic pelvic pain, and infertility. However, the molecular mechanisms involved in adenomyosis development remain unclear. This paper summarizes the reports found in the MEDLINE database on the molecular mechanisms involved in the development and progression of uterine adenomyosis. The literature search included the following terms: "adenomyosis," "adenomyoma," "pathogenesis," "molecular mechanisms," and "gynecological disorders." Only peer-reviewed, English-language journal articles were included. This review focuses on the molecular genetics, epigenetic modifications, and pivotal signaling pathways associated with adenomyosis development and progression, which will provide insights into and a better understanding of its underlying pathophysiology.

• Genomics & Informatics
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• v.19 no.1
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• pp.2.1-2.10
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• 2021

BRAF inhibitors (e.g., vemurafenib) are widely used to treat metastatic melanoma with the BRAF V600E mutation. The initial response is often dramatic, but treatment resistance leads to disease progression in the majority of cases. Although secondary mutations in the mitogen-activated protein kinase signaling pathway are known to be responsible for this phenomenon, the molecular mechanisms governing acquired resistance are not known in more than half of patients. Here we report a genome- and transcriptome-wide study investigating the molecular mechanisms of acquired resistance to BRAF inhibitors. A microfluidic chip with a concentration gradient of vemurafenib was utilized to rapidly obtain therapy-resistant clones from two melanoma cell lines with the BRAF V600E mutation (A375 and SK-MEL-28). Exome and transcriptome data were produced from 13 resistant clones and analyzed to identify secondary mutations and gene expression changes. Various mechanisms, including phenotype switching and metabolic reprogramming, have been determined to contribute to resistance development differently for each clone. The roles of microphthalmia-associated transcription factor, the master transcription factor in melanocyte differentiation/dedifferentiation, were highlighted in terms of phenotype switching. Our study provides an omics-based comprehensive overview of the molecular mechanisms governing acquired resistance to BRAF inhibitor therapy.

• Journal of Ginseng Research
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• v.46 no.2
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• pp.214-224
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• 2022

Red ginseng oil (RGO), rather than the conventional aqueous extract of red ginseng, has been receiving much attention due to accumulating evidence of its functional and pharmacological potential. In this review, we describe the key extraction technologies, chemical composition, potential health benefits, and safety of RGO. This review emphasizes the proposed molecular mechanisms by which RGO is involved in various bioactivities. RGO is mainly produced using organic solvents or supercritical fluid extraction, with the choice of method greatly affecting the yield and quality of the end products. RGO contains a high unsaturated fatty acid levels along with considerable amounts of lipophilic components such as phytosterols, tocopherols, and polyacetylenes. The beneficial health properties of RGO include cellular defense, antioxidation, anti-inflammation, anti-apoptosis, chemoprevention, hair growth promotion, and skin health improvement. We propose several molecular mechanisms and signaling pathways that underlie the bioactivity of RGO. In addition, RGO is regarded as safe and nontoxic. Further studies on RGO must focus on a deeper understanding of the underlying molecular mechanisms, composition-functionality relationship, and verification of the bioactivities of RGO in clinical models. This review may provide useful information in the development of RGO-based products in nutraceuticals, functional foods, and functional cosmetics.

• Microbiology and Biotechnology Letters
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• v.19 no.1
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• pp.100-108
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• 1991

Molecular characteristics and improving methods for thermal stability of enzyme have been considered. Intrinsic and extrinsic stabilizing mechanisms are two governing principles for enhanced thermal stability of enzyme in molecular basis. Factors contributing to the former and the latter mechanisms may be involved in the enhanced thermal stability of enzyme complementarily. Also, the methods for improving thermal stability of enzyme which comprise reaction in organic solvent system, chemical modification, immobilization, sequential unfolding and refolding, gene manipulation techniques and enzyme-antibody complexing are reviewed.

• Environmental Mutagens and Carcinogens
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• v.26 no.4
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• pp.97-112
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• 2006

Heme oxygenase(HO)-1 is an important antioxidant enzyme that plays a pivotal role in cellular adaptation and protection in response to a wide array of noxious stimuli. Thus, HO-1 induction has been associated with prevention or mitigation of pathogenesis of various diseases, including acute inflammation, atherosclerosis, degenerative diseases, and carcinogenesis. Recent progress in our understanding of the function of molecules in the cellular signaling network as key modulators of gene transcription sheds light on the molecular mechanisms underlyuing HO-1 gene expression. A panel of redox-sensitive transcription factors such as activator protein-1, nuclear factor-kB, and nuclear factor E2-related factor-2, and some of the upstream kinases have been identified as prime regulators of HO-1 gene induction. This review summarizes molecular mechanisms underlying HO-1 expression and the significance of targeted induction of HO-1 as a potential chemopreventive or chemoprotective strategy.

• Toxicological Research
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• v.17
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• pp.205-210
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• 2001

One of the major focuses and perhaps the greatest challenges during the past decade in the discipline of immunotoxicology has been the elucidation of the molecular mechanisms responsible for immunotoxicity by specific agents. Much is currently understood about the basic underlying intracellular processes that control leukocyte effector function. This fundamental information in cell biology can now be applied toward developing systematic approaches, through the application of cell and molecular biology techniques, to identify the intracellular targets and processes disrupted by immunotoxicants. The objective of this paper is two fold. First to discuss fundamental principles of experimental design aimed at elucidation of cellular mechanisms in immunotoxicology; and second to discuss the application of molecular biology techniques in characterizing the mechanism of TCDD-induced B cell dysfunction as a working example.

• 한국생물공학회:학술대회논문집
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• 2005.04a
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• pp.530-530
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• 2005

• Molecules and Cells
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• v.41 no.1
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• pp.3-10
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• 2018

Autophagy is one of the major degradative mechanisms that can eliminate excessive nutrients, toxic protein aggregates, damaged organelles and invading microorganisms. In response to obesity and obesity-associated lipotoxic, proteotoxic and oxidative stresses, autophagy plays an essential role in maintaining physiological homeostasis. However, obesity and its associated stress insults can often interfere with the autophagic process through various mechanisms, which result in further aggravation of obesity-related metabolic pathologies in multiple metabolic organs. Paradoxically, inhibition of autophagy, within specific contexts, indirectly produces beneficial effects that can alleviate several detrimental consequences of obesity. In this minireview, we will provide a brief discussion about our current understanding of the impact of obesity on autophagy and the role of autophagy dysregulation in modulating obesity-associated pathological outcomes.

• BMB Reports
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• v.50 no.4
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• pp.186-193
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• 2017

In mammals, cap-dependent translation of mRNAs is initiated by two distinct mechanisms: cap-binding complex (CBC; a heterodimer of CBP80 and 20)-dependent translation (CT) and eIF4E-dependent translation (ET). Both translation initiation mechanisms share common features in driving cap- dependent translation; nevertheless, they can be distinguished from each other based on their molecular features and biological roles. CT is largely associated with mRNA surveillance such as nonsense-mediated mRNA decay (NMD), whereas ET is predominantly involved in the bulk of protein synthesis. However, several recent studies have demonstrated that CT and ET have similar roles in protein synthesis and mRNA surveillance. In a subset of mRNAs, CT preferentially drives the cap-dependent translation, as ET does, and ET is responsible for mRNA surveillance, as CT does. In this review, we summarize and compare the molecular features of CT and ET with a focus on the emerging roles of CT in translation.

• Preventive Nutrition and Food Science
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• v.22 no.2
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• pp.81-89
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• 2017

Healthy aging has become a major goal of public health. Many studies have provided evidence and theories to explain molecular mechanisms of the aging process. Recent studies suggest that epigenetic mechanisms are responsible for life span and the progression of aging. Epigenetics is a fascinating field of molecular biology, which studies heritable modifications of DNA and histones that regulate gene expression without altering the DNA sequence. DNA methylation is a major epigenetic mark that shows progressive changes during aging. Recent studies have investigated aging-related DNA methylation as a biomarker that predicts cellular age. Interestingly, growing evidence proposes that nutrients play a crucial role in the regulation of epigenetic modifiers. Because various nutrients and their metabolites function as substrates or cofactors for epigenetic modifiers, nutrition can modulate or reverse epigenetic marks in the genome as well as expression patterns. Here, we will review the results on aging-associated epigenetic modifications and the possible mechanisms by which nutrition, including nutrient availability and bioactive compounds, regulate epigenetic changes and affect aging physiology.