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C-fos

Glover, J.N.M., Harrison, S.C. Crystal structure of the het-erodimeric bZIP transcription factor c-Fos-c-Jun bound to DNA. Nature 373 257-261, 1995. [Pg.203]

The time required to eool the pilot plant bateh reaetor is 0.85 hr. Applying form II of Equation 13-67 and C) fo "... [Pg.1063]

Immediate early genes, e.g., c-fos, c-jun, and c-myc, are the first genes whose expression is induced in cells after a growth stimulus. They encode transcription factors and induce the expression of other growth-related genes. [Pg.612]

Quinone-mono-ketals 46 and 47 are also low reactive dienophiles and are sensitive to Lewis-acid catalysts. The use of high pressure overcomes this limitation [17]. As shown in Equation 5.7, cycloadditions with a variety of substituted 1,3-butadienes 48 occur regioselectively and c This approach provides access to a variety of annulated benzenes and naphthalenes after aromatization of adducts 49. [Pg.212]

Gubits, R.M. Fairhurst, J.L. (1988). c-fos mRNA levels are increased by the cellular stressors, heat shock and sodium arsenite. Oncogene 3, 163-168. [Pg.454]

Ryabinin AE, Criado JR, Henriksen SJ, et al Differential sensitivity of c-Fos expression in hippocampus and other brain regions to moderate and low doses of alcohol. Mol Psychiatry 2 32 3, 1997... [Pg.52]

The developed chromatogram is dried in a stream of cold air, immersed in the dippini solution for 2 s, then dried in a stream of warm air for 5 min and heated to 110°C fo 1-2 min until the coloration reaches its maximum. [Pg.820]

Second, although typical neuroleptics produce depolarisation block of both A9 and AlO neurons, the atypical neuroleptics only induce it in AlO neurons (Chiodi and Bunney 1983). So after an atypical neuroleptic the A9 neurons of the nigrostriatal tract remain functional, which would explain why EPSs are not seen. Another difference is seen with the expression of an immediate-early gene, c-fos, and although its functional significance is not clear, typical neuroleptics induce its protein production in both the striatum and nucleus accumbens while the atypicals only achieve it in the accumbens. [Pg.362]

There is certainly evidence that whereas typical neuroleptics are equally active in mesolimbic/cortical areas as well as the striatum, the atypical drugs are much less effective in the latter. This has been shown by (1) increased DA turnover through DOPAC and HVA production in vitro, (2) augmented DA and DOPAC release by microdialysis in vivo and (3) increased c-fos- ike, expression. [Pg.364]

Measuring the expression of the early-immediate gene c-fos supports the striatal role of neuroleptics in the induction of EPSs because although all neuroleptics induce such expression in both the nucleus accumbens and striatum, the atypical neuroleptics do so more in the accumbens while clozapine, but not risperidone, also achieve it in the prefrontal cortex (Robertson, Matsumura and Fibiger 1994). How this arises is uncertain but since risperidone is a more potent 5-HT2 antagonist than clozapine, it cannot be through that mechanism. [Pg.370]

Subsequent studies have confirmed that the reason for this discrepancy is that the rat is able to rapidly metabolise P-carotene to retinol in the intestine, through the action of intestinal dioxygenase. In contrast humans absorb P-carotene systemically such that plasma levels of P-carotene increase to levels not found in the rodent. A more appropriate animal model is the ferret, which shows a similar metabolism to humans. High levels of plasma P-carotene in the ferret induce the cellular transcription factors c-fos and c-jun, and squamous metaplasia is seen in the lung with or without exposure to cigarette smoke (SCF, 2000). Even after the investment of all these resources it has not been possible for the EU Scientific Committee on Food to set an ADI. [Pg.230]

Basset-S6guin, N., Escot, C., Blanchard, J.M., Kerai, C., Verrier, B., Moin, H. and Guilhou, J.J. (1990). High levels of c-fos proto-oncogene expression in normal human adult skin. J. Invest. Dermatol. 94, 418-422. [Pg.120]

Dudley C.A. and Moss R.L. (1994). Lesions of the accessory olfactory bulb decrease lordotic responsiveness and reduce mating-induced c-fos expression in the accessory olfactory system. Brain Res 642, 29-37. [Pg.201]

Guo J., Zhou A. and Moss R. (1997). Urine and urine-derived compounds induce c-fos mRNA expression in accessory olfactory bulb. Neuroreport 8, 1679-1683. [Pg.209]

Kollack-Walker S. and Newman S.W. (1997). Mating-induced expression of c-fos in the male Syrian hamster brain role of experience, pheromones, and ejaculations. Neurobiol J 32, 481-501. [Pg.220]

Schellinck H., Smyth C., Brown R. and Wilkinson M. (1993). Odor-induced sexual maturation and expression of c-fos in the olfactory system of juvenile female mice. Dev Brain Res 74, 138-141. [Pg.245]

Shyamala V, Khoja H. Interleukin-8 receptors R1 and R2 activate mitogen-activated protein kinases and induce c-fos, independent of Ras and Raf-1 in Chinese hamster ovary cells. Biochemistry 1998 37(45) 15918-15924. [Pg.330]


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