Cyclic GMP (cGMP), produced in response to either nitric oxide (NO) or certain peptides, controls important neuronal functions. NG108-15 cells were used to characterize the expression of NO- and cGMP-generating proteins and to identify potential alterations associated with neuronal differentiation (neurite outgrowth). We find that these cells contain exclusively neuronal NO synthase (nNOS) isoforms as well as both NO- (soluble guanylyl cyclase, sGC) and natriuretic peptide- (natriuretic peptide receptor-A, NPR-A) responsive cGMP-producing enzymes.
View Article and Find Full Text PDFObjectives: To investigate androgen receptor (AR) function in spinal and bulbar muscular atrophy (SBMA).
Methods: A kindred was identified with five individuals carrying the AR gene CAG repeat expansion that causes SBMA. Androgen binding was measured in cultured genital skin fibroblasts from three affected individuals.
Identification of androgen-regulated genes in neurons is an important step in understanding the mechanisms involved in androgen action. The aim of the current study was to identify androgen-responsive genes in the neural cells using the technique of differential display reverse transcription polymerase chain reaction (DDRT-PCR) on the human neuroblastoma cell line, SK-N-MC. Using this analysis, 18 putatively androgen-regulated cDNA species were identified, ranging in size from 280 to 800 bp.
View Article and Find Full Text PDFMol Cell Endocrinol
January 2004
Differential activation of PKC isoforms by angiotensin II (AII) has been found in a variety of tissues in which this important octapeptide mediates its multitude of effects. To date, the PKC isoforms involved in mediating brain-specific effects are yet to be defined. In the present study, the identity of PKC isoforms coupled to AII stimulation was examined in the neuroblastoma X glioma hybrid cell line, NG108-15, by Western blot analysis.
View Article and Find Full Text PDFKennedy's disease (spinobulbar muscular atrophy) is an X-linked form of motor neuron disease affecting adult males carrying a CAG trinucleotide repeat expansion within the androgen receptor gene. While expression of Kennedy's disease is thought to be confined to males carrying the causative mutation, subclinical manifestations have been reported in a few female carriers of the disease. The reasons that females are protected from the disease are not clear, especially given that all other diseases caused by CAG expansions display dominant expression.
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