CREB-binding protein (CBP) is a transcriptional coactivator whose mutations may cause a generalized perturbation of gene expression. We silenced the CBP gene in NT2 neuronal precursor cells by RNA interference. Hybridization experiments on 1.2K human cDNA microarrays showed that the FSCN1 gene, encoding for fascin-1 protein, was clearly less expressed in CBP-depleted cells than in controls. This reduction was confirmed by Real Time PCR and Western blotting assays. We also analyzed FSCN1 expression profile during NT2 neuronal differentiation induced by retinoic acid (RA), showing that FSCN1 was up-regulated during neurogenesis. This mRNA increasing suggests the importance of fascin-1 in the formation of mature neurons, in accordance with its actin-bundling function and its localization in neurites and neuronal growth cones. The lower amount of FSCN1 transcript in the absence of the CBP factor was also established in RA-treated cells. In conclusion, this research supports FSCN1 as a novel marker of NT2 neuronal differentiation and the possible role of CBP in its regulation.
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http://dx.doi.org/10.1016/j.neulet.2005.02.027 | DOI Listing |
Int J Mol Sci
September 2024
Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia.
J Clin Sleep Med
September 2024
Department of Systems Medicine, University of Rome Tor Vergata, Italy.
Int J Immunogenet
October 2024
Department of Clinical Sciences, Malmö, Lund University, Malmo, Sweden.
Narcolepsy is a sleep disorder caused by an apparent degeneration of orexin/hypocretin neurons in the lateral hypothalamic area and a subsequent decrease in orexin/hypocretin levels in the cerebrospinal fluid. Narcolepsy is classified into type 1 (NT1) and type 2 (NT2). While genetic associations in the human leukocyte antigen (HLA) region and candidate autoantibodies have been investigated in NT1 to imply an autoimmune origin, less is known about the pathogenesis in NT2.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
June 2024
Department of Human Genetics, University of Miami, Miller School of Medicine, Sylvester Comprehensive Cancer Center, Miami, FL 33136.
Repressor element-1 silencing transcription factor (REST) is required for the formation of mature neurons. REST dysregulation underlies a key mechanism of neurodegeneration associated with neurological disorders. However, the mechanisms leading to alterations of REST-mediated silencing of key neurogenesis genes are not known.
View Article and Find Full Text PDFCell Death Discov
May 2024
Department of Chemistry and Biochemistry, Worcester Polytechnic Institute, Worcester, Massachusetts, 01609, USA.
The Gα/phospholipase C-β (PLCβ) signaling system mediates calcium responses to a variety of hormones and neurotransmitters. Recent studies suggest that PLCβ1 expression plays a role in the differentiation of two types of cultured neuronal cells (PC12 and SK-N-SH) through a mechanism independent of Gα. Here, we show that, similar to that observed in PC12 and SK-N-SH cells, PLCβ1 expression increases when human NT2 cells are induced to differentiate either through cytosine-β-D-arabinofuranoside or retinoic acid.
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