• Asian Pacific Journal of Cancer Prevention
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• 제16권8호
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• pp.3085-3090
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• 2015

The telomeric end structures of the DNA are known to contain tandem repeats of TTAGGG sequence bound with specialised protein complex called the "shelterin complex". It comprises six proteins, namely TRF1, TRF2, TIN2, POT1, TPP1 and RAP1. All of these assemble together to form a complex with double strand and single strand DNA repeats at the telomere. Such an association contributes to telomere stability and its protection from undesirable DNA damage control-specific responses. However, any alteration in the structure and function of any of these proteins may lead to undesirable DNA damage responses and thus cellular senescence and death. In our review, we throw light on how mutations in the proteins belonging to the shelterin complex may lead to various malfunctions and ultimately have a role in tumorigenesis and cancer progression.

• BMB Reports
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• 제41권11호
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• pp.751-756
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• 2008

Aging and cancer both occur as a result of accumulated cellular damage, and both are related to the regulation of specific genes in the damage response. Recent research has unveiled connections between the mechanisms of aging and cancer, but how to prevent the development of cancer and increase longevity remain unknown. SIRT1 (the mammalian Sir2), which has $NAD^+$-dependent class III histone deacetylase activity, may be a key gene linking the modulation of cancer and aging. SIRT1 has broad biological functions in growth regulation, stress response, tumorigenesis, endocrine signaling, and extended lifespan. Here, we focus on the current knowledge regarding the role of SIRT1 in aging and cancer, and discuss the implications of SIRT1 as a therapeutic target for the optimal balance between anti-aging and anti-cancer activities.

• Biomolecules & Therapeutics
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• 제17권2호
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• pp.113-124
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• 2009

Aging is a multifaceted biological process that affects all organs and organ systems of the body. This review provides an up-to-date analysis of this highly exciting, rapidly changing field of science. The aging process is largely under genetic control but is highly responsive to diverse environmental influences. The genes that control aging are those that are involved with cell maintenance, cell damage and repair. The environmental factors that accelerate aging are those that influence either damage of cellular macromolecules, or interfere with their repair. Prominent among these are chronic inflammation, chronic infection, some metallic chemicals, ultraviolet light, and others that heighten oxidative stress. Other environment factors slow the aging process. Included among these agents are resveratrol and vitamin D. In addition, dietary restriction and exercise have been found to extend human lifespan. The various mechanisms whereby all these agents exert their influence on aging include epigenetic modification, chromatin maintenance, protection of telomeres, and anti-oxidant defense, among others. The complex process of aging remains under continued, intense investigation.

• International Journal of Industrial Entomology and Biomaterials
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• 제43권2호
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• pp.94-98
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• 2021

Reactive oxygen species (ROS) induce a variety of cellular responses, such as proliferation, differentiation, senescence, and apoptosis. Intestinal epithelial cells are continuously exposed to ROS, and excessive generation of ROS severely damages cells via oxidative stress. Pro-inflammatory cytokines may lead to intestinal inflammation and damage by inducing excessive ROS generation. In this study, we showed that papiliocin, an antimicrobial peptide, significantly inhibited ROS production, without affecting cell viability. Moreover, TNF-α and IL-6 expression was decreased in the intestinal epithelial cells. The activity of papiliocin may significantly contribute to preserving the integrity of the intestinal mucosa against oxidative damage and inflammation-related disorders.

• Biomolecules & Therapeutics
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• 제31권5호
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• pp.559-565
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• 2023

Ataxia-telangiectasia mutated (ATM), a master kinase of the DNA damage response (DDR), phosphorylates a multitude of substrates to activate signaling pathways after DNA double-strand breaks (DSBs). ATM inhibitors have been evaluated as anticancer drugs to potentiate the cytotoxicity of DNA damage-based cancer therapy. ATM is also involved in autophagy, a conserved cellular process that maintains homeostasis by degrading unnecessary proteins and dysfunctional organelles. In this study, we report that ATM inhibitors (KU-55933 and KU-60019) provoked accumulation of autophagosomes and p62 and restrained autolysosome formation. Under autophagy-inducing conditions, the ATM inhibitors caused excessive autophagosome accumulation and cell death. This new function of ATM in autophagy was also observed in numerous cell lines. Repression of ATM expression using an siRNA inhibited autophagic flux at the autolysosome formation step and induced cell death under autophagy-inducing conditions. Taken together, our results suggest that ATM is involved in autolysosome formation and that the use of ATM inhibitors in cancer therapy may be expanded.

• 한국응용과학기술학회지
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• 제32권4호
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• pp.781-788
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• 2015

본 연구에서는 건조된 까마중(Solanum nigrum L.) 전초의 50% 에탄올 추출물, 에틸아세테이트 분획, 아글리콘 분획을 이용하여 항산화 실험을 진행하였다. 1,1-diphenyl-2-picrylhydrazyl(DPPH)을 이용한 자유라디칼 소거 활성($FSC_{50}$)은 50% 에탄올 추출물, 에틸아세테이트 분획, 아글리콘 분획에서 각각 $215.46{\mu}g/mL$, $42.43{\mu}g/mL$, $52.28{\mu}g/mL$이였다. Luminol-의존성 화학발광법을 이용한 $Fe^{3+}-EDTA/H_2O_2$ 계에서의 총항산화능($OSC_{50}$) 평가에서, 까마중 50% 에탄올 추출물은 $25.25{\mu}g/mL$, 에틸아세테이트 분획은 $7.05{\mu}g/mL$, 아글리콘 분획은 $6.25{\mu}g/mL$를 나타냈다. $^1O_2$로 유도된 적혈구 세포손상에 대한 보호효과 측정에서는 까마중 50% 에탄올 추출물 및 아글리콘 분획은 $5{\sim}25{\mu}g/mL$ 농도에서는 세포보호효과를 나타냈으나 높은 농도에서는 세포보호 활성을 나타내지 않았다. 이러한 결과를 통해 까마중 추출물 및 분획물들은 항산화 활성을 가지고 있지만, 세포 수준에서는 비교적 높은 농도에서 활성산소로 유도된 세포 손상을 촉진할 수도 있음을 시사한다. 따라서 화장품 등에 까마중 추출물을 응용할 때는 사용상 주의가 필요한 것으로 판단된다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.94-94
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• 2002

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimer's disease (AD). Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.115-115
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• 2001

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimers disease (AD). Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• Journal of Applied Biological Chemistry
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• 제43권4호
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• pp.211-217
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• 2000

Oxidative stress is implicated in a number of diseases, in ageing of organisms, and in damage to plants that have been exposed to freezing and thawing or water stress. From the perspective of yeast as a model eukaryotic system, this article reviews the systems that are involved in the cellular responses to exposure to reactive oxygen species (ROS) generated during aerobic growth of the organism. The discussion includes the defense systems involved, the ability of cells to adapt to ROS treatment, cell-division cycle delay and the systems regulating gene expression that are activated by oxidative stress.

• 한국어업기술학회:학술대회논문집
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• 한국어업기술학회 2001년도 춘계 수산관련학회 공동학술대회발표요지집
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• pp.97-98
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• 2001

Alpha-tocopherol (alpha-Toc) is a classical lipophilic antioxidant well known as a scavenger of free radicals in a hydrophobic milieu. The primary function of alpha-Toc is to stabilize cellular and subcellar membrane by preventing peroxidative damage of structural polyunsaturated fatty acids (PUFA). The characteristic aroma of sweet smelt Precoglossun altivelis is known as oxida breakdown products of PUFA ironically. (omitted)