ArticleCellular and molecular neurobiology2006
Voltage-dependent N-type Ca2+ channel activity regulates the interaction between FGF-1 and S100A13 for stress-induced non-vesicular release.
Article in Cellular and molecular neurobiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Non-Vesicular Release of Alarmin Prothymosin α Complex Associated with Annexin-2 Flop-Out.Cells · 2023Review
- Involvement of SNARE Protein Interaction for Non-classical Release of DAMPs/Alarmins Proteins, Prothymosin Alpha and S100A13.Cellular and molecular neurobiology · 2021Article
- Article
- Topically Applied Etamsylate: A New Orphan Drug for HHT-Derived Epistaxis (Antiangiogenesis through FGF Pathway Inhibition).TH open : companion journal to thrombosis and haemostasis · 2019Article
- Protein folding does not prevent the nonclassical export of FGF1 and S100A13.Biochemical and biophysical research communications · 2009Article
- Prothymosin alpha plays a key role in cell death mode-switch, a new concept for neuroprotective mechanisms in stroke.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- Secretion without Golgi.Journal of cellular biochemistry · 2008Review
- Structure of calcium-bound human S100A13 at pH 7.5 at 1.8 A resolution.Acta crystallographica. Section F, Structural biology and crystallization communications · 2008Article
- Crystallization and preliminary X-ray analysis of human S100A13.Acta crystallographica. Section F, Structural biology and crystallization communications · 2006Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The Ca(2+)-mediated regulation of interaction between FGF-1 and S100A13 in NG108-15 cells was studied. When the stress by depriving B27 supplement from the culture was given, cellular levels of both proteins were decreased, while their releases were significantly increased within 3 h. These stress-induced changes were all abolished by amlexanox, an anti-allergic drug. 2. These releases were significantly inhibited by the addition of EGTA or BAPTA-AM, cellular or extracellular Ca(2+)-chelating agent, respectively. The addition of omega-conotoxin GVIA, a N-type Ca(2+)-channel blocker caused a complete inhibition of the release, while increased the cytosolic levels of both proteins. However, omega-conotoxin MVIIC, the non-N-type Ca(2+)-channel blocker was ineffective. 3. In NG108-15 cells, which had been transfected with Venus-FGF-1 and CFP-S100A13, the supplement-deprivation stress caused several spike-type fluorescence resonance energy transfer (FRET) signals, suggesting that both proteins showing interaction would be immediately released. These spikes were completely abolished by the addition of omega-conotoxin GVIA. However, the addition of amlexanox caused bell-shaped FRET signals without spikes. 4. Thus, it is suggested that the interaction between FGF-1 and S100A13 responsible for stress-induced non-vesicular release is dependent of Ca(2+)-influx through N-type Ca(2+)-channels.
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