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001-es BibID:	BIBFORM094330
Első szerző:	Varga Zoltán (biofizikus, szakfordító)
Cím:	The Kv1.3 K+ channel in the immune system and its "precision pharmacology" using peptide toxins / Varga Zoltan, Tajti Gabor, Panyi Gyorgy
Dátum:	2021
ISSN:	2676-8615 2676-8607
Megjegyzések:	Since the discovery of the Kv1.3 voltage-gated K+ channel in human T cells in 1984, ion channels are considered crucial elements of the signal transduction machinery in the immune system. Our knowledge about Kv1.3 and its inhibitors is outstanding, motivated by their potential application in autoimmune diseases mediated by Kv1.3 overexpressing efector memory T cells (e.g., Multiple Sclerosis). High afnity Kv1.3 inhibitors are either small organic molecules (e.g., Pap-1) or peptides isolated from venomous animals. To date, the highest afnity Kv1.3 inhibitors with the best Kv1.3 selectivity are the engineered analogues of the sea anemone peptide ShK (e.g., ShK-186), the engineered scorpion toxin HsTx1[R14A] and the natural scorpion toxin Vm24. These peptides inhibit Kv1.3 in picomolar concentrations and are several thousand-fold selective for Kv1.3 over other biologically critical ion channels. Despite the signifcant progress in the feld of Kv1.3 molecular pharmacology several progressive questions remain to be elucidated and discussed here. These include the conjugation of the peptides to carriers to increase the residency time of the peptides in the circulation (e.g., PEGylation and engineering the peptides into antibodies), use of rational drug design to create novel peptide inhibitors and understanding the potential of-target efects of Kv1.3 inhibition.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Kv1.3 Toxin Mutation Increase in selectivity Pharmacological tailoring
Megjelenés:	Biologia Futura. - 72 : 1 (2021), p. 75-83. -
További szerzők:	Tajti Gábor (1988-) (gyógyszerész, biofizikus, sejtbiológus) Panyi György (1966-) (biofizikus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00015 GINOP EFOP-3.6.2-16-2017-00006 EFOP K119417 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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