Expression of Fos, Jun, and Krox family proteins in Alzheimer's disease
- PMID: 9344557
- DOI: 10.1006/exnr.1997.6600
Expression of Fos, Jun, and Krox family proteins in Alzheimer's disease
Abstract
Apoptosis is an active process of cell death characterized by distinct morphological features and is often the end result of a genetic program of events, i.e., programmed cell death (PCD). There is growing evidence supporting a role for apoptosis and/or PCD in Alzheimer's disease (AD), based on DNA fragmentation studies and recent findings of increased levels of inducible transcription factors (ITFs) such as c-Jun in AD brains. We have characterized the expression of a large range of ITFs (c-Fos, Fos B, Fos-related antigens, c-Jun, Jun B, Jun D, Krox20, and Krox24) using multiple antisera in AD postmortem hippocampi and compared this with human control hippocampi as well as Huntington's disease hippocampi and human epilepsy biopsy tissue. We found little evidence of nuclear expression of any ITF except c-Jun in the human postmortem tissue, compared with nuclear staining in biopsy tissue. We found some evidence for increased levels of c-Jun and Krox24 protein and krox24 mRNA in the CA1 region of AD hippocampi, suggesting that PCD may be involved in the pathogenesis of AD. In general, staining characteristics of ITFs varied with different antisera directed against the same protein, indicating the need for caution when interpreting results.
Similar articles
-
Basal expression of the inducible transcription factors c-Jun, JunB, JunD, c-Fos, FosB, and Krox-24 in the adult rat brain.J Comp Neurol. 1995 Mar 27;354(1):39-56. doi: 10.1002/cne.903540105. J Comp Neurol. 1995. PMID: 7615874
-
Effects of amphetamine and cocaine treatment on c-Fos, Jun-B, and Krox-24 expression in rats with intrastriatal dopaminergic grafts.Exp Neurol. 1999 Sep;159(1):139-52. doi: 10.1006/exnr.1999.7129. Exp Neurol. 1999. PMID: 10486183
-
NMDA receptor overstimulation triggers a prolonged wave of immediate early gene expression: relationship to excitotoxicity.Exp Neurol. 1997 Apr;144(2):406-15. doi: 10.1006/exnr.1997.6427. Exp Neurol. 1997. PMID: 9168840
-
The regulation of c-fos: too much is never enough.Adv Second Messenger Phosphoprotein Res. 1993;28:271-7. Adv Second Messenger Phosphoprotein Res. 1993. PMID: 8398414 Review. No abstract available.
-
Neuronal expression of AP-1 proteins in excitotoxic-neurodegenerative disorders and following nerve fiber lesions.Prog Neurobiol. 1995 Nov-Dec;47(4-5):257-90. Prog Neurobiol. 1995. PMID: 26445738 Review.
Cited by
-
Epileptogenesis in the immature brain: emerging mechanisms.Nat Rev Neurol. 2009 Jul;5(7):380-91. doi: 10.1038/nrneurol.2009.80. Nat Rev Neurol. 2009. PMID: 19578345 Free PMC article. Review.
-
Enhancer-driven gene regulatory networks inference from single-cell RNA-seq and ATAC-seq data.Brief Bioinform. 2024 Jul 25;25(5):bbae369. doi: 10.1093/bib/bbae369. Brief Bioinform. 2024. PMID: 39082647 Free PMC article.
-
Uncovering molecular biomarkers that correlate cognitive decline with the changes of hippocampus' gene expression profiles in Alzheimer's disease.PLoS One. 2010 Apr 13;5(4):e10153. doi: 10.1371/journal.pone.0010153. PLoS One. 2010. PMID: 20405009 Free PMC article.
-
Age-dependent changes in TDP-43 levels in a mouse model of Alzheimer disease are linked to Aβ oligomers accumulation.Mol Neurodegener. 2010 Nov 11;5:51. doi: 10.1186/1750-1326-5-51. Mol Neurodegener. 2010. PMID: 21070634 Free PMC article.
-
Alzheimer's disease and brain development: common molecular pathways.Front Biosci. 1998 Jan 15;3:d100-12. doi: 10.2741/a267. Front Biosci. 1998. PMID: 9422711 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous