149 results on '"Dekan, Zoltan"'
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2. Production, composition, and mode of action of the painful defensive venom produced by a limacodid caterpillar, Doratifera vulnerans
3. A tetrapeptide class of biased analgesics from an Australian fungus targets the μ-opioid receptor
4. Novel Scorpion Toxin ω-Buthitoxin-Hf1a Selectively Inhibits Calcium Influx via Ca V 3.3 and Ca V 3.2 and Alleviates Allodynia in a Mouse Model of Acute Postsurgical Pain.
5. PHAB toxins: a unique family of predatory sea anemone toxins evolving via intra-gene concerted evolution defines a new peptide fold
6. The α1-adrenoceptor inhibitor ρ-TIA facilitates net hunting in piscivorous Conus tulipa
7. Anti-allodynic effects of the selective NaV1.7 inhibitor Pn3a in a mouse model of acute post-surgical pain: evidence for analgesic synergy with opioids and baclofen
8. Antiallodynic effects of the selective NaV1.7 inhibitor Pn3a in a mouse model of acute postsurgical pain: evidence for analgesic synergy with opioids and baclofen
9. Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain
10. The Tarantula Toxin ω-Avsp1a Specifically Inhibits Human CaV3.1 and CaV3.3 via the Extracellular S3-S4 Loop of the Domain 1 Voltage-Sensor
11. Cysteine-Rich α-Conotoxin SII Displays Novel Interactions at the Muscle Nicotinic Acetylcholine Receptor
12. Multitarget nociceptor sensitization by a promiscuous peptide from the venom of the King Baboon spider
13. The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel NaV1.8 to Enhance Activation
14. The Tarantula Toxin ω-Avsp1a Specifically Inhibits Human Ca V 3.1 and Ca V 3.3 via the Extracellular S3-S4 Loop of the Domain 1 Voltage-Sensor.
15. Nature-inspired dimerization as a strategy to modulate neuropeptide pharmacology exemplified with vasopressin and oxytocin
16. Synthesis and In vitro Biological Activity of Cyclic Lipophilic χ-Conotoxin MrIA Analogues
17. Mutational analysis of ProTx-I and the novel venom peptide Pe1b provide insight into residues responsible for selective inhibition of the analgesic drug target NaV1.7
18. The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel NaV1.8 to Enhance Activation.
19. Isolation, characterization and total regioselective synthesis of the novel μO-conotoxin MfVIA from Conus magnificus that targets voltage-gated sodium channels
20. It Takes Two: Dimerization Is Essential for the Broad-Spectrum Predatory and Defensive Activities of the Venom Peptide Mp1a from the Jack Jumper Ant Myrmecia pilosula
21. Addition of K22 Converts Spider Venom Peptide Pme2a from an Activator to an Inhibitor of NaV1.7
22. Mapping the Molecular Surface of the Analgesic NaV1.7-Selective Peptide Pn3a Reveals Residues Essential for Membrane and Channel Interactions
23. Fulditoxin, representing a new class of dimeric snake toxins, defines novel pharmacology at nicotinic ACh receptors
24. Novel venom-derived inhibitors of the human EAG channel, a putative antiepileptic drug target
25. The α1-adrenoceptor inhibitor ρ-TIA facilitates net hunting in piscivorous Conus tulipa.
26. Development and Application of a Peptide Inhibitor-Bound Quantum Dot Targeting the Voltage-Gated Potassium Channel KV1.3 in the Olfactory Bulb
27. Conotoxin Φ‐MiXXVIIA from the Superfamily G2 Employs a Novel Cysteine Framework that Mimics Granulin and Displays Anti‐Apoptotic Activity
28. Modulatory features of the novel spider toxin μ‐TRTX‐Df1a isolated from the venom of the spider Davus fasciatus
29. Δ‐Myrtoxin‐Mp1a is a Helical Heterodimer from the Venom of the Jack Jumper Ant that has Antimicrobial, Membrane‐Disrupting, and Nociceptive Activities
30. Correction: Corrigendum: Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a
31. Novel Human Eag Channel Antagonists from Spider Venoms
32. Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a
33. Development of a μO-Conotoxin Analogue with Improved Lipid Membrane Interactions and Potency for the Analgesic Sodium Channel NaV1.8
34. Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain
35. Rational Design and Synthesis of a Novel Membrane Binding NaV1.8 Selective Inhibitor with in vivo Activity in Pain Models
36. Xenopus borealis as an alternative source of oocytes for biophysical and pharmacological studies of neuronal ion channels
37. Identification and Characterization of ProTx-III [μ-TRTX-Tp1a], a New Voltage-Gated Sodium Channel Inhibitor from Venom of the Tarantula Thrixopelma pruriens
38. A Tarantula-Venom Peptide Antagonizes the TRPA1 Nociceptor Ion Channel by Binding to the S1–S4 Gating Domain
39. Total Synthesis of Human Hepcidin through Regioselective Disulfide-Bond Formation by using the Safety-Catch Cysteine Protecting Group 4,4′-Dimethylsulfinylbenzhydryl
40. Selenoether oxytocin analogues have analgesic properties in a mouse model of chronic abdominal pain
41. Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain.
42. Development of aμO-Conotoxin Analogue with Improved Lipid Membrane Interactions and Potency for the Analgesic Sodium Channel NaV1.8.
43. Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain.
44. Conotoxin engineering: dual pharmacophoric noradrenaline transport inhibitor/integrin binding peptide with improved stability
45. α-Conotoxin ImI Incorporating Stable Cystathionine Bridges Maintains Full Potency and Identical Three-Dimensional Structure
46. Modulating Oxytocin Activity and Plasma Stability by Disulfide Bond Engineering
47. Synthesis and In vitroBiological Activity of Cyclic Lipophilic χ-Conotoxin MrIA Analogues
48. Corrigendum: Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a.
49. The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel Na V 1.8 to Enhance Activation.
50. Mapping the Molecular Surface of the Analgesic Na V 1.7-Selective Peptide Pn3a Reveals Residues Essential for Membrane and Channel Interactions.
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