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Nerve growth factor -treated

Like the estrogen levels, so the total testosterone level and the bioavailable testosterone level, in particular, decline in both sexes with age. Testosterone supplementation was reported to protect orchiectomized, aging male rats from osteoporosis (260), increase nerve growth factor levels in rat brain (261), or improve depression in aging men (262). The treatment of N2a cells and rat primary cere-brocortical neurons with testosterone increased secretion of sAPPa and diminished the release of A 3s (263). In a similar manner, treatment of GTl-7 rat hypothalamic cells with testosterone stimulated the a-secretory pathway by increasing the secretion of sAPPa, without affecting the total amount of cellular APP (216). In a group of six men treated for adenocarcinoma of the prostate with hormonal suppressants, the precipitous drop in their levels of testosterone and estradiol correlated with the increase of A/340 plasma levels (264). The therapeutic implications of observations like these remain uncertain. [Pg.766]

Houle, J. D. and Johnson, J. E., Nerve growth factor (NGF)-treated nitrocellulose enhances and directs the regeneration of adult rat dorsal root axons through intraspinal neural tissue transplants, Neurosci. Lett., 103, 17, 1989. [Pg.196]

Nerve gr<)wlh J(iclt)r pathway. Nerve-growth factor (NGF) binds tn a protein tyrosine kina.se receptor. T he amount of diacylglycerol in the plasma membrane increases in cells expressing this receptor when treated with NGF. Propose a simple signaling pathway and identify the isoform of any participating enzymes. Would you expect the concentrations of any other common second messengers to increase on NGF treatment. ... [Pg.406]

Pioro EP, Ribeiro-da-Silva A, Cuello AC (1991) Similarities in tbe ultrastructural distribution of nerve growth factor receptor-like immunoreactivity in cerebellar Purkinje cells of the neonatal and colchicine-treated adult rat. J. Comp. Neurol, 305, 189-200. [Pg.354]

Kami-untan-to (KUT) > Kampo traditional preparation for treating age-related memory loss and dementia. oral administration increased choline acetyltransferase activity in frontoparietal cortex and reduced cognitive impairment in forebrain-lesioned rats. KUT indirectly increases available achetylcholine by inducing increased transcription of choline acetyltransferase (ChAT) and Nerve Growth Factor (NGF) mRNA. putative mechanism is stimulated NGF production resulting in increased ChAT production, and indirectly, increased Acetylcholine production (ACh). [Pg.1120]

An increase in glucose utilization and in the biosynthesis of lipids, proteins, and RNA has been observed in ganglia which were treated with the factor. A rise of RNA synthesis precedes the increase of protein synthesis. Actinomycin D abolishes the effect of nerve growth factor on protein synthesis (Levi-Montalcini, 1967). [Pg.285]

Eigure 4.6 shows a representative topographical image of undifferentiated (i.e., no treatment of nerve growth factor, NGE) and differentiated (NGF-treated) PC12 cells (model neurons) recorded... [Pg.59]

Y. Ihara, Y. Sakamoto, M. Mihara, K. Shimizu, N. Taniguchi, Overexpression of N-acetyl-glucosaminyltransferase III disrupts the tyrosine phosphorylation of Trk with resultant signaling dysfunction in PC 12 cells treated with nerve growth factor, J Biol Chem, 1997, 272, 9629-9634. [Pg.1288]


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Nerve growth factor

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