Data

Data from: Chemical engineering and structural and pharmacological characterization of the alpha-scorpion toxin OD1

RMIT University, Australia
Professor David J Adams (Associated with, Aggregated by)
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ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Adc&rfr_id=info%3Asid%2FANDS&rft_id=https://figshare.com/articles/Chemical_Engineering_and_Structural_and_Pharmacological_Characterization_of_the_Scorpion_Toxin_OD1/2402908&rft.title=Data from: Chemical engineering and structural and pharmacological characterization of the alpha-scorpion toxin OD1&rft.identifier=384afb55aa5c2b3e2736a793a8e5bb0c&rft.publisher=RMIT University, Australia&rft.description=Attached file provides supplementary data for linked article. Scorpion alpha-toxins are invaluable pharmacological tools for studying voltage-gated sodium channels, but few structure-function studies have been undertaken due to their challenging synthesis. To address this deficiency, we report a chemical engineering strategy based upon native chemical ligation. The chemical synthesis of alpha-toxin OD1 was achieved by chemical ligation of three unprotected peptide segments. A high resolution X-ray structure (1.8 angstrom) of synthetic OD1 showed the typical beta alpha beta beta alpha-toxin fold and revealed important conformational differences in the pharrnacophore region when compared with other alpha-toxin structures. Pharmacological analysis of synthetic OD1 revealed potent alpha-toxin activity (inhibition of fast inactivation) at Na(v)1.7, as well as Na(v)1.4 and Na(v)1.6. In addition, OD1 also produced potent beta-toxin activity at Na(v)1.4 and Na(v)1.6 (shift of channel activation in the hyperpolarizing direction), indicating that ODI might interact at more than one site with Na(v)1.4 A and Na(v)1.6. Investigation of nine OD1 mutants revealed that three residues in the reverse turn contributed significantly to selectivity, with the triple ODI mutant (D9K, D10P, K11H) being 40 fold more selective for Na(v)1.7 over Na(v)1.6, while OD1 K11V was 5-fold more selective for Na1.6(v) than Na(v)1.7. This switch in selectivity highlights the importance of the reverse turn for engineering alpha-toxins with altered selectivity at Na-v subtypes.&rft.creator=Professor David J Adams&rft.date=2018&rft.relation=http://dx.doi.org/10.1021/cb400012k&rft_rights=All rights reserved&rft_rights=CC BY-NC: Attribution-Noncommercial 3.0 AU http://creativecommons.org/licenses/by-nc/3.0/au&rft_subject=Gated sodium channels&rft_subject=Expression&rft_subject=Androctonus australis hector&rft_subject=Odonthobuthus doriae&rft_subject=Neurotoxin&rft_subject=Protein&rft_subject=Modulation&rft_subject=Activation&rft_subject=Mechanisms &rft_subject=Inhibition&rft_subject=Basic Pharmacology&rft_subject=MEDICAL AND HEALTH SCIENCES&rft_subject=PHARMACOLOGY AND PHARMACEUTICAL SCIENCES&rft.type=dataset&rft.language=English Access the data

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Attached file provides supplementary data for linked article. Scorpion alpha-toxins are invaluable pharmacological tools for studying voltage-gated sodium channels, but few structure-function studies have been undertaken due to their challenging synthesis. To address this deficiency, we report a chemical engineering strategy based upon native chemical ligation. The chemical synthesis of alpha-toxin OD1 was achieved by chemical ligation of three unprotected peptide segments. A high resolution X-ray structure (1.8 angstrom) of synthetic OD1 showed the typical beta alpha beta beta alpha-toxin fold and revealed important conformational differences in the pharrnacophore region when compared with other alpha-toxin structures. Pharmacological analysis of synthetic OD1 revealed potent alpha-toxin activity (inhibition of fast inactivation) at Na(v)1.7, as well as Na(v)1.4 and Na(v)1.6. In addition, OD1 also produced potent beta-toxin activity at Na(v)1.4 and Na(v)1.6 (shift of channel activation in the hyperpolarizing direction), indicating that ODI might interact at more than one site with Na(v)1.4 A and Na(v)1.6. Investigation of nine OD1 mutants revealed that three residues in the reverse turn contributed significantly to selectivity, with the triple ODI mutant (D9K, D10P, K11H) being 40 fold more selective for Na(v)1.7 over Na(v)1.6, while OD1 K11V was 5-fold more selective for Na1.6(v) than Na(v)1.7. This switch in selectivity highlights the importance of the reverse turn for engineering alpha-toxins with altered selectivity at Na-v subtypes.

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