• Molecules and Cells
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• v.46 no.11
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• pp.664-671
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• 2023

The proper maintenance of mRNA quality that is regulated by diverse surveillance pathways is essential for cellular homeostasis and is highly conserved among eukaryotes. Here, we review findings regarding the role of mRNA quality control in the aging and longevity of Caenorhabditis elegans, an outstanding model for aging research. We discuss the recently discovered functions of the proper regulation of nonsense-mediated mRNA decay, ribosome-associated quality control, and mRNA splicing in the aging of C. elegans. We describe how mRNA quality control contributes to longevity conferred by various regimens, including inhibition of insulin/insulin-like growth factor 1 (IGF-1) signaling, dietary restriction, and reduced mechanistic target of rapamycin signaling. This review provides valuable information regarding the relationship between the mRNA quality control and aging in C. elegans, which may lead to insights into healthy longevity in complex organisms, including humans.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.5
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• pp.1677-1682
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• 2015

Cancer progression is attained by uncontrolled cell division and metastasis. Increase in tumor size triggers different vascular channel formation to address cell nutritional demands. These channels are responsible for transferring of nutrients and gaseous to the cancer cells. Cancer vascularization is regulated by numerous factors including vascular endothelial growth factors (VEGFs). These factors play an important role during embryonic development. Members included in this group are VEGFA, VEGFB, VEGFC, PIGF and VEGFD which markedly influence cellular growth and apoptosis. Being freely diffusible these proteins act in both autocrine and paracrine fashions. In this review, genetic characterization these molecules and their putative role in cancer staging has been elaborated. Prognostic significance of these molecules along with different stages of cancer has also been summarized. Brief outline of ongoing efforts to target hot spot target sites against these VEGFs and their cognate limitations for therapeutic implications are also highlighted.

• Journal of the Korean institute of surface engineering
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• v.17 no.2
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• pp.29-40
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• 1984

The structure of rapidly solidified Al-Si-based alloys and its relationship to subsequent anodic film growth in near neutral and acid solutions have been investigated. Solidification of the alloys proceeds via pre-dendritic nuclei, associated with rugosity of the casting surface, from which cellular-type growth, comprised of aluminium-rich material surrounded by silicon-containing material, emanates. Observation of ultramicrotomed sections of the alloys and their anodic films reveals the local oxidation of the silicon-rich phase and its incorporation into the anodic alumina film, formed in near neutral solutions. Such incorporation occurs but resultant isolation of the silicon-rich phase is not possible for anodizing in phosphoric acid, and a three-dimensional network of the oxidized silicon-containing phase, with continuing development of porous anodic alumina, is observed.

• BMB Reports
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• v.36 no.1
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• pp.49-59
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• 2003

Platelet-derived growth factor (PDGF) is a critical regulator of mesenchymal cell migration and proliferation. The vital functions of PDGFs for angiogenesis, as well as development of kidney, brain, cardiovascular system and pulmonary alveoli during embryogenesis, have been well demonstrated by gene knock-out approaches. Clinical studies reveal that aberrant expression of PDGF and its receptor is often associated with a variety of disorders including atherosclerosis, fibroproliferative diseases of lungs, kidneys and joints, and neoplasia. PDGF contributes to cancer development and progression by both autocrine and paracrine signaling mechanisms. In this review article, important features of the PDGF isoforms and their cell surface receptor subunits are discussed, with regards to signal transduction, PDGF-isoform specific cellular response, and involvement in angiogenesis, and tumorstromal interactions.

• Biomedical Science Letters
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• v.21 no.2
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• pp.126-130
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• 2015

There are several studies that show hypothermia improves cellular ischemia damages on experimental and clinical bases. However, its exact molecular mechanisms are unclear. In this study, we demonstrate that hypothermia induced insulin-like growth factor 1 (IGF1) gene expression, and its expression was dramatically decreased under ischemic insults. It was also demonstrated that hypothermia activated endoplasmic reticulum (ER) stress sensors especially both the phosphorylation of $eIF2{\alpha}$ (eukaryotic translation initiation factor 2 alpha) and ATF6 (activating transcription factor-6) proteolytic cleavage. However, the factors of apoptosis and autophagy were not associated with hypothermia. We suggest that hypothermia-treated IGF1 gene expression after ischemia may show a good possibility for the development of treatments and diagnostic methods in cerebral ischemic damages.

• Proceedings of the Materials Research Society of Korea Conference
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• 2011.10a
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• pp.2.1-2.1
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• 2011

Biomedical applications of electrospun nanofibrous meshes have been receive tremendous attentions because of their unique structures and versatilities as novel biomaterials. Incorporation of growth factors in fibrous meshes can be performed by surface-modification and encapsulation. Those growth factors stimulate differentiation and proliferation of specific types of cells and thus lead tissue regenerations of specific cell types. Topographical cues of electrospun nanofibrous meshes also increase differentiation of specific cell types according to alignments of fibrous structures. Wound healing treatments of diabetic ulcers were performed using nanofibrous meshes encapsulating multiple growth factors. Aligned nanofibrous meshes and those with random configuration were compared for differentiating mesenchymal stem cells into neuronal cells. Thus, nanofibrous meshes can be applied to novel drug delivery carriers and matrix for promoting cellular proliferation.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.133-133
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• 2001

It is well known that p38 mitogen-activated protein kinase (p38MAPK) participates in cellular responses to mitogenic stimuli, environmental and genotoxic stresses, and apoptotic agents. Although there are several reports on p38MAPK in relation to cell growth and apoptosis, the exact mechanism of p38MAPK-mediated cell growth regulation remains obscure.(omitted)

• Journal of Microbiology and Biotechnology
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• v.10 no.5
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• pp.606-611
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• 2000

Dimorphic yeast Candida albicans reversibly switches between the form of yeast and hyphae depending on external conditions. We investigated possible roles of the myosin family in the growth and dimorphic switches of C. albicans with a general myosin ATPase inhibitor, 2,3-butanedione-2-monoxime (BDM). Transition to hyphae as well as proliferation by budding was completely inhibited by BDM at 16 mM. Presence of 16 mM BDM did not affect hyphae-to-bud transition but it blocked budding. The effects of BDM on yeast growth and dimorphic switches were reversible. More than 70% of the BDM-treated cells demonstrated defects in the amount and the polarized localization of F-actin as well as in the shape and migration of the nucleus, suggesting that myosin activities are needed in these cellular processes of C. albicans.

• 연구논문집
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• s.23
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• pp.15-27
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• 1993

The single crystal specimens were solidified by modified Bridgeman method. The surface recrystallized single crystal specimens were prepared by shot peening followed by heat treatment. The surface recrystallization begins at the dendrite cores on the surface. The recrystallized grains grew into the inner side of the specimen. The growth of recrystallized grains was inhibited by the pores and eutectic phases. The primary $\gamma'$ phases were dissolved at the recrystallized grain boundaries during the grain growth. The grain growth of recrystallized grains was similar to the cellular type transformation. No orientation relationships were found bewteen the recrystallized grains and the parent phase.

• Archives of Pharmacal Research
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• v.26 no.3
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• pp.183-191
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• 2003

Nucleic acid therapies represent a direct genetic approach for cancer treatment. Such an approach takes advantage of mechanisms that activate genes known to confer a growth advantage to neoplastic cells. The ability to block the expression of these genes allows exploration of normal growth regulation. Progress in antisense technology has been rapid, and the traditional antisense inhibition of gene expression is now viewed on a genomic scale. This global view has led to a new vision in antisense technology, the elimination of nonspecific and undesirable side effects, and ultimately, the generation of more effective and less toxic nucleic acid medicines. Several antisense oligonucleotides are in clinical trials, are well tolerated, and are potentially active therapeutically. Antisense oligonucleotides are promising molecular medicines for treating human cancer in the near future.