ArticleCellular and molecular life sciences : CMLS2009
Calcium signaling-induced Smad3 nuclear accumulation induces acetylcholinesterase transcription in apoptotic HeLa cells.
Article in Cellular and molecular life sciences : CMLS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Two Fluorescent Probes for Recognition of Acetylcholinesterase: Design, Synthesis, and Comparative Evaluation.Molecules (Basel, Switzerland) · 2024Article
- AChE for DNA degradation.Cell research · 2015Article
- Nesprin-2 mediated nuclear trafficking and its clinical implications.Nucleus (Austin, Tex.) · 2015Article
- Acetylcholinesterase involvement in apoptosis.Frontiers in molecular neuroscience · 2012Article
- ATP induces synaptic gene expressions in cortical neurons: transduction and transcription control via P2Y1 receptors.Molecular pharmacology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
Recently, acetylcholinesterase (AChE) has been studied as an important apoptosis regulator. We previously showed that cellular calcium mobilization upregulated AChE expression by modulating promoter activity and mRNA stability. In this study, we have identified a potential Smad3/4 binding element, TGCCAGACA, located within the -601 to -571 bp fragment of the AChE promoter, as an important calcium response motif. Smad2/3 and Smad4 were shown to bind this element. Overexpression of human Smad3 increased AChE transcription activity in a dose-dependent manner in HeLa cells, whereas dominant-negative Smad3 blocked this activation. Upon A23187 and thapsigargin treatment, nuclear Smad3 accumulation was observed, an effect that was blocked by the intracellular Ca(2+) chelator BAPTA-AM. Calcium-induced AChE transcriptional activation was significantly blocked when the nuclear localization signal of Smad3 was destroyed. Taken together, our data suggest Smad3 can regulate AChE transcriptional activation following calcium-induced nuclear accumulation.
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Registered trials
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