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发布于:2020-11-27 08:14:22  访问:0 次 回复:0 篇
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Compound Bow Arrows
Colocalization of nitroguanine and iNOS was found in oral epithelium of patients with OLP, OSCC and leukoplakia.Immunoreactivity of nitrotyrosine, which is formed by protein tyrosine nitration and considered to be a biochemical marker for inflammation, was also observed in oral epithelial cells.Accumulation of p was observed in oral epithelium in OLP and leukoplakia, and more prominent expression of this protein was observed in OSCC patients.It is concluded that the formation of nitroguanine and oxodG may contribute to the development of oral cancer from OLP and leukoplakia.DNA damage was specifically induced at sites of carcinogenesis under various inflammatory conditions.In hamsters infected with the liver fluke OV causing cholangiocarcinoma, nitroguanine formation was induced in bile duct epithelium. Moreover, nitroguanine was formed in colonic gland epithelial cells in a mouse model of IBD. It is noteworthy that nitroguanine formation was also observed in human samples.Therefore, nitroguanine could be used as a potential biomarker of inflammationrelated carcinogenesis.Establishment of methods for quantitative analysis of nitroguanine in biological or clinical specimens could be useful for evaluating the risk of carcinogenesis.However, nitroguanine formed in DNA is chemically unstable, and this characteristic may hamper its quantitative analysis.Therefore, free nitroguanine released from DNA in urine might be available for quantification as a biomarker.In addition, measurement of nitroguanosine derived from nitroguaninebound RNA in clinical specimens, including white blood cells, may be useful for evaluation of carcinogenic potential.Recently, nitroguanosine has been reported to be a highly redoxactive molecule. More importantly, experimental evidence has suggested that nitroguanine is a mutagenic DNA lesion, which preferentially leads to GT transversions, in addition to oxodG. Indeed, GT transversions have been observed in vivo in the ras gene and the p tumor suppressor gene in lung and liver cancer. These findings imply that DNA damage mediated by ROS and RNS may participate in carcinogenesis via activation of protooncogenes and inactivation of tumor suppressor genes.Infection with liver flukes. Carcinogenesis. Gastroenterology. Biochemistry. Carcinogenesis. J. Pharmacol. Sci. View publication stats View publication stats Expression of the mdm gene is stimulated by p and this reciprocal relationship forms the basis of a negative feedback loop.Both genotoxic and nongenotoxic stresses that induce p focus principally on interruption of the pMDM loop with the consequence that p becomes stabilised, leading to changes in the expression of presponsive genes.The biological endpoints of p induction are growth arrest, which can be transient or permanent, or apoptosis.The number of physiological p responsive genes is likely to run into hundreds, but intensive studies have so far established direct roles for only a small group of players in mediating the p response.It is therefore envisioned that their expression and individual functions contribute to a coordinated series of events and that additional key contributions from other responsive genes are likely to be important.There are also believed to be other, ptransactivationindependent mechanisms that contribute to apoptosis including the ability of p to repress gene expression.MDM is an E ubiquitin ligase which, together with the p transcriptional coactivator protein, mediates both the ubiquitylation and buy Psoralen proteasomedependent degradation of p. MDM can also mediate translocation of p to the cytoplasm thereby removing it from its site of action, and can D.
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