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ht ease clustering and homo-dimerization, which in turn might affect signaling. The signaling role of PTN is not well investigated. We speculate that the presence of PTN might be necessary for the effects of Y-P30 on ectodomain shedding or prevention of SDC cleavage. The association of both peptides with SDC might occur also in other tissues and with other family members like SDC-1 and -4. Along these lines it was indeed shown that Y-P30 is expressed in breast cancer and that ectodomain shedding of SDC might be causally related to a poor prognosis in this and potentially other types of cancer. At present it is unclear whether the Y-P30 peptide might play a role PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19652232 during neuronal development in human brain. The expression of Y-P30 mRNA has been reported in human brain regions. However, recent reports indicate that the human Y-P30/ dermcidin peptide as well as the mRNA are extremely stable for several weeks and can be used as abundant markers for human sweat in forensic medicine. Thus, the contamination of cell cultures and tissue sections during processing by human skin in analogy to keratin is a serious concern in all studies looking at YP30 expression. In light of the difficulties to identify a rodent YP30/dermcidin gene it is therefore conceivable that reports by us and potentially also of others on the presence of the peptide in rodents are confounded by contaminations with the human peptide. Conclusion The survival promoting peptide Y-P30 promotes neurite outgrowth in a manner that involves SDC/Cask signaling. Interference with the nuclear localization of CASK using the peptide might be of interest for pharmacological applications to promote neurite outgrowth and cell survival. Organisms are constantly exposed to the influence of adverse environmental factors. Among the most common adverse influences are formaldehyde, toluene, dioxins and low dose of ionizing radiation. Exposure to ionizing radiation in low doses causes stochastic effects and often leads to harmful longterm consequences in humans . Formaldehyde is one of the most reactive pollutants, and has a wide range of household and industrial sources,. Acute and chronic exposure to formaldehyde has many health effects, such as allergies, neuro- toxicity, pulmonary function damage, hematotoxicity, reproductive toxicity, genotoxicity, carcinogenesis, etc.. Dioxins are persistent organic pollutants that are emitted from the incineration of solid waste and polyvinyl chloride, combustion of wood, automobile emissions, etc. and accumulated in soil and water and are able to be accumulated in the human body. They are the most potent synthetic poisons, being effective even at trace concentrations. Toluene is an ingredient in organic solvents and dyes, and comes into MRT-67307 cost contact with inhaled air. Toluene is an irritant capable of affecting the central nervous system and causing metabolic acidosis,. Even at low concentrations, toluene causes oxidative stress and genotoxicity. 1 Gene Expression after Radiation and Pollutants In recent years, dozens of papers have been published studying the expression of various genes under the action of dioxins, formaldehyde,, toluene, and ionizing radiation. In this work, we compare the transcriptional signatures of four adverse factors in order to show exposure and sex-specific effects, based on our own experimental data. We investigate which cell response mechanisms induced by the pollutants are common to the different factors. This will expand our under

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Author: heme -oxygenase