Activation of Human Monoamine Oxidase B Gene Expression by a Protein Kinase C MAPK Signal Transduction Pathway Involves c-Jun and Egr-1 *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 277, Issue: 25, Page: 22222-22230
2002
- 70Citations
- 23Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations70
- Citation Indexes69
- 69
- CrossRef56
- Patent Family Citations1
- Patent Families1
- Captures23
- Readers23
- 23
Article Description
Monoamine oxidases (MAO) A and B deaminate a number of biogenic amines. Aberrant expression of MAO is implicated in several psychiatric and neurogenerative disorders. In this study, we have shown that phorbol 12-myristate 13-acetate (PMA) increases human MAO B, but not MAO A, gene expression. The sequence between −246 and −225 bp consists of overlapping binding sites (Sp1/Egr-1/Sp1) that are recognized by Sp1, Sp3, and PMA-inducible Egr-1 is essential for PMA activation. PMA transiently increases egr-1 and c- jun gene expression. Mutation studies show that Egr-1 and c-Jun transactivate the MAO B promoter and increase endogenous MAO B transcripts via the Sp1/Egr-1/Sp1 overlapping binding sites. Sp3 inhibits Sp1 and Egr-1 activation of MAO B gene expression. c- fos gene expression was increased by PMA but not involved in MAO B gene transcription. Furthermore, protein kinase C inhibitor blocks the PMA-dependent activation of MAO B. Co-transfection of the MAO B promoter with dominant negative forms of Ras, Raf-1, MEKK1, MEK1, MEK3, MEK7, ERK2, JNK1, and p38/RK inhibit the PMA-dependent activation of the MAO B promoter. These results indicate that MAO B expression is selectively induced by the activation of protein kinase C and MAPK signaling pathway and that c-Jun and Egr-1 appear to be the ultimate targets of this regulation.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925819668067; http://dx.doi.org/10.1074/jbc.m202844200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0037151015&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11956220; http://www.jbc.org/lookup/doi/10.1074/jbc.M202844200; https://syndication.highwire.org/content/doi/10.1074/jbc.M202844200; https://linkinghub.elsevier.com/retrieve/pii/S0021925819668067; https://dx.doi.org/10.1074/jbc.m202844200; http://www.jbc.org/article/S0021925819668067/abstract; http://www.jbc.org/article/S0021925819668067/fulltext; http://www.jbc.org/article/S0021925819668067/pdf; https://www.jbc.org/article/S0021-9258(19)66806-7/abstract; http://www.jbc.org/cgi/doi/10.1074/jbc.M202844200; http://www.jbc.org/content/277/25/22222.abstract; http://www.jbc.org/content/277/25/22222.full; http://www.jbc.org/content/277/25/22222.full.pdf; http://www.jbc.org/content/277/25/22222; http://www.jbc.org/content/early/2002/04/15/jbc.M202844200; http://www.jbc.org/content/early/2002/04/15/jbc.M202844200.full.pdf; https://www.jbc.org/content/277/25/22222
American Society for Biochemistry & Molecular Biology (ASBMB)
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