• Title/Summary/Keyword: Cytosolic

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Expression of Glutathione Reductase Gene in Transgenic Tobacco Plant (형질전환 담배 식물체에서 Glutathione Reductase 유전자의 발현)

  • 이효신;조진기
    • Korean Journal of Plant Tissue Culture
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    • v.28 no.2
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    • pp.87-90
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    • 2001
  • BcGRl gene encoding cytosolic glutathione reductase of Chinese cabbage (Brassica campestris var. Pekinensis cv. Seoul) was placed under the control of the CaMV 35S promoter and introduced into tobacco (Nicotiana tabacum L. cv. Samsun) via Agrobacterium-mediated transformation. T$_{0}$ 32 independent plants transformed with BcGRl gene were selected with kanamycin and they were confirmed by polymerase chain reaction (PCR) and Southern blot analysis. Northern blot analysis revealed that the constitutive expression of BcGRl gene and there was no relationship between the copy number of introduced gene and the levels of BcGRl transcripts.

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Mitochondrial DNA Somatic Mutation in Cancer

  • Kim, Aekyong
    • Toxicological Research
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    • v.30 no.4
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    • pp.235-242
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    • 2014
  • Cancer cells are known to drastically alter cellular energy metabolism. The Warburg effect has been known for over 80 years as pertaining cancer-specific aerobic glycolysis. As underlying molecular mechanisms are elucidated so that cancer cells alter the cellular energy metabolism for their advantage, the significance of the modulation of metabolic profiles is gaining attention. Now, metabolic reprogramming is becoming an emerging hallmark of cancer. Therapeutic agents that target cancer energy metabolism are under intensive investigation, but these investigations are mostly focused on the cytosolic glycolytic processes. Although mitochondrial oxidative phosphorylation is an integral part of cellular energy metabolism, until recently, it has been regarded as an auxiliary to cytosolic glycolytic processes in cancer energy metabolism. In this review, we will discuss the importance of mitochondrial respiration in the metabolic reprogramming of cancer, in addition to discussing the justification for using mitochondrial DNA somatic mutation as metabolic determinants for cancer sensitivity in glucose limitation.

Identification of a 68 kDa cytosolic. neutral and Mg2+-independent Sphingomyelinase by MALDI- TOF Analysis

  • Seo, Young-Deog;Park, Hong-Jun;Hyun, Myung-Han;Cho, Dong-Hwan;Jung, Sung-Yun;Kim, Dae-Kyong
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.291.1-291.1
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    • 2002
  • A cytosolic. neutral and magnesium-independent Sphingomyelinase (N-cSMase) is known to playa role in vitamin D3-induced differentiation and neurodegeneration such as Alzheimer's disease and stroke through the production of ceramide. a lipid-derived tumor suppressive mediator. However. little is known about its identity and characteristics. (omitted)

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Deciphering Macrophage Phenotypes upon Lipid Uptake and Atherosclerosis

  • Jihye Lee;Jae-Hoon Choi
    • IMMUNE NETWORK
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    • v.20 no.3
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    • pp.22.1-22.21
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    • 2020
  • In the progression of atherosclerosis, macrophages are the key immune cells for foam cell formation. During hyperlipidemic condition, phagocytic cells such as monocytes and macrophages uptake oxidized low-density lipoproteins (oxLDLs) accumulated in subintimal space, and lipid droplets are accumulated in their cytosols. In this review, we discussed the characteristics and phenotypic changes of macrophages in atherosclerosis and the effect of cytosolic lipid accumulation on macrophage phenotype. Due to macrophage plasticity, the inflammatory phenotypes triggered by oxLDL can be re-programmed by cytosolic lipid accumulation, showing downregulation of NF-κB activation followed by activation of anti-inflammatory genes, leading to tissue repair and homeostasis. We also discuss about various in vivo and in vitro models for atherosclerosis research and next generation sequencing technologies for foam cell gene expression profiling. Analysis of the phenotypic changes of macrophages during the progression of atherosclerosis with adequate approach may lead to exact understandings of the cellular mechanisms and hint therapeutic targets for the treatment of atherosclerosis.