Pub. Date : 1997 Mar 7
PMID : 9098543
10 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Cryptic brain cell injury caused by fetal nicotine exposure is associated with persistent elevations of c-fos protooncogene expression. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 2 | In the current study, pregnant rats were given nicotine by implanted minipump infusion either from gestational days 4-12 or 4-21 and fetal and neonatal brain regions were examined for expression of the mRNA encoding c-fos, a nuclear transcription factor that becomes chronically elevated when cell injury or apoptosis are occurring. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 3 | In contrast to the elevation of c-fos seen with prenatal nicotine, postnatal nicotine injections given to 2-day-old rats did not cause acute stimulation of c-fos expression. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 4 | The ability of injected nicotine to evoke acute rises in c-fos emerged by postnatal day 8 and initially displayed regional specificity paralleling the concentration of nicotinic cholinergic receptors. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 5 | With increasing maturity, regional selectivity of the c-fos response to acute nicotine was lost, consistent with indirect actions that could be mediated through nicotine-induced hypoxia/ischemia. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 6 | These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 7 | These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 8 | These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 9 | Given that chronic elevations of c-fos are known to be associated with cell injury and to evoke apoptosis in otherwise healthy cells, these results suggest that prenatal nicotine exposure evokes delayed neurotoxicity by altering the program of neural cell differentiation, and that elevated c-fos expression provides an early marker of the eventual deficits. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |
| 10 | Given that chronic elevations of c-fos are known to be associated with cell injury and to evoke apoptosis in otherwise healthy cells, these results suggest that prenatal nicotine exposure evokes delayed neurotoxicity by altering the program of neural cell differentiation, and that elevated c-fos expression provides an early marker of the eventual deficits. | Nicotine | Fos proto-oncogene, AP-1 transcription factor subunit | Rattus norvegicus |