siRNA-mediated silencing of the gene for heat shock transcription factor 1 causes hypersensitivity to methylmercury in HEK293 cells

Hwang, Gi Wook; Ryoke, Katsunori; Lee, Jin Yong; Takahashi, Tsutomu; Naganuma, Akira

doi:10.2131/jts.36.851

Cited by 9 publications

(9 citation statements)

References 14 publications

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“…Furthermore, the research group led by Dr. Naganuma has found a large number of proteins that are resistant or hypersensitive to MeHg (Hwang et al, 2007(Hwang et al, , 2010a(Hwang et al, , 2010b(Hwang et al, , 2010c(Hwang et al, , 2011b(Hwang et al, , 2012a(Hwang et al, , 2012b(Hwang et al, , 2013b. For example, they found that L-glutamine:D-fructose-6-phosphate amidotransferase (GFAT), which is an essential enzyme for catalyzing the synthesis of glucosamine-6-phosphate from glutamine and fructose-6-phosphate, is a factor that confers MeHg-resistance and that GFAT is the intracellular target molecule for MeHg toxicity Naganuma et al, 2000).…”

Section: Attempts To Identify Cases Of the S-mercuration Of Proteinsmentioning

confidence: 99%

S-Mercuration of cellular proteins by methylmercury and its toxicological implications

2014

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-The accumulation of methylmercury (MeHg) through the daily consumption of large predatory fish poses potential health risks. MeHg has been found to cause Minamata disease, but the full nature of MeHg toxicity remains unclear. Because of its chemical properties, MeHg covalently binds to cellular proteins through their reactive thiols, referred to as S-mercuration, resulting in the formation of protein adducts. In this review, we summarize how the S-mercuration of cellular proteins could be involved in the major mechanisms that have been suggested to underlie MeHg toxicity. Additionally, we introduce our attempts to identify cases of S-mercuration for the research to reveal the true nature of MeHg toxicity.

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Section: Attempts To Identify Cases Of the S-mercuration Of Proteinsmentioning

confidence: 99%

S-Mercuration of cellular proteins by methylmercury and its toxicological implications

2014

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“…The siRNA-transfected cells were plated into single wells of 12-well plates and cultured for 72 hr. Total RNA was isolated using Isogen reagent (Nippon gene, Tokyo, Japan) according to the manufacturer's protocol (Hwang et al, 2010(Hwang et al, , 2011. First strand cDNA was synthesized using the PrimeScript TM RT reagent kit (Takara, Shiga, Japan).…”

Section: Sirna Transfection and Quantitative Real-time Pcrmentioning

confidence: 99%

Increased production of reactive oxygen species by the vacuolar-type (H+)-ATPase inhibitors bafilomycin A1 and concanamycin A in RAW 264 cells

Yokomakura

Hong²,

Ohuchi³

et al. 2012

J. Toxicol. Sci.

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-Treatment of the mouse leukemic cell line RAW 264 with bafilomycin A1 or concanamycin A, inhibitors of vacuolar-type (H + )-ATPases (V-ATPases), significantly increased the production of reactive oxygen species (ROS) and decreased cell viability. These effects were significantly suppressed by the presence of N-acetyl cysteine (NAC), an ROS scavenger. si-RNA mediated knockdown of the gene for the c subunit of the V0 domain of V-ATPase also resulted in an increase in ROS production and a decrease in cell viability. These results suggest that decreased cellular V-ATPase activity decreases cell viability by increasing ROS production in RAW 264 cells.

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“…As well, correlations between high expression of HSF1 mRNA with cancer grade, metastasis, and poor prognosis suggest that it has a role in tumor progression. Several examples of the effect of silencing this gene in different cancer types have been revealing an increase of apoptosis, a reduction or inhibition of the tumor growth, a decrease in cancer cells proliferation, and an inhibition of cellular transformation and tumorigenesis, once more attesting its relevance in cancer disease [68,71,72,73]. …”

Section: Combinatory Approachesmentioning

confidence: 99%

Gold Nanoparticle Approach to the Selective Delivery of Gene Silencing in Cancer—The Case for Combined Delivery?

Mendes

Fernandes

Baptista

2017

Genes

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Gene therapy arises as a great promise for cancer therapeutics due to its potential to silence genes involved in tumor development. In fact, there are some pivotal gene drivers that suffer critical alterations leading to cell transformation and ultimately to tumor growth. In this vein, gene silencing has been proposed as an active tool to selectively silence these molecular triggers of cancer, thus improving treatment. However, naked nucleic acid (DNA/RNA) sequences are reported to have a short lifetime in the body, promptly degraded by circulating enzymes, which in turn speed up elimination and decrease the therapeutic potential of these drugs. The use of nanoparticles for the effective delivery of these silencers to the specific target locations has allowed researchers to overcome this issue. Particularly, gold nanoparticles (AuNPs) have been used as attractive vehicles for the target-specific delivery of gene-silencing moieties, alone or in combination with other drugs. We shall discuss current trends in AuNP-based delivery of gene-silencing tools, considering the promising road ahead without overlooking existing concerns for their translation to clinics.

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siRNA-mediated silencing of the gene for heat shock transcription factor 1 causes hypersensitivity to methylmercury in HEK293 cells

Cited by 9 publications

References 14 publications

<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

Increased production of reactive oxygen species by the vacuolar-type (H<sup>+</sup>)-ATPase inhibitors bafilomycin A1 and concanamycin A in RAW 264 cells

Gold Nanoparticle Approach to the Selective Delivery of Gene Silencing in Cancer—The Case for Combined Delivery?

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