ArticlePloS one2013
δ/ω-Plectoxin-Pt1a: an excitatory spider toxin with actions on both Ca(2+) and Na(+) channels.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- A venom fraction from the Philippine tarantula (The journal of venomous animals and toxins including tropical diseases · 2026Article
- Towards a Sustainable Management of the Spotted-Wing Drosophila: Disclosing the Effects of Two Spider Venom Peptides onInsects · 2023Article
- Not so Dangerous After All? Venom Composition and Potency of the Pholcid (Daddy Long-Leg) SpiderFrontiers in ecology and evolution · 2019Article
- Protein Palmitoylation and Its Role in Bacterial and Viral Infections.Frontiers in immunology · 2017Review
- Plectreurys tristis venome: A proteomic and transcriptomic analysis.Journal of venom research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The venom of spider Plectreurys tristis contains a variety of peptide toxins that selectively target neuronal ion channels. O-palmitoylation of a threonine or serine residue, along with a characteristic and highly constrained disulfide bond structure, are hallmarks of a family of toxins found in this venom. Here, we report the isolation and characterization of a new toxin, δ/ω-plectoxin-Pt1a, from this spider venom. It is a 40 amino acid peptide containing an O-palmitoylated Ser-39. Analysis of δ/ω-plectoxin-Pt1a cDNA reveals a small precursor containing a secretion signal sequence, a 14 amino acid N-terminal propeptide, and a C-terminal amidation signal. The biological activity of δ/ω-plectoxin-Pt1a is also unique. It preferentially blocks a subset of Ca(2+) channels that is apparently not required for neurotransmitter release; decreases threshold for Na(+) channel activation; and slows Na(+) channel inactivation. As δ/ω-plectoxin-Pt1a enhances synaptic transmission by prolonging presynaptic release of neurotransmitter, its effects on Na(+) and Ca(2+) channels may act synergistically to sustain the terminal excitability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.