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001-es BibID:	BIBFORM132699
035-os BibID:	(scopus)105020160474 (wos)001603700400001
Első szerző:	Borrego, Jesús
Cím:	Modulators of the Human Voltage-Gated Proton Channel Hv1 / Borrego Jesús, Mészáros Beáta, Szanto Tibor G., Teshome Russo Teklu, Korpos Éva, Varga Zoltan, Papp Ferenc
Dátum:	2025
ISSN:	1424-8247
Megjegyzések:	The voltage-gated proton channel (Hv1) selectively transports protons (H+) across biological membranes in response to membrane potential changes. Hv1 is assembled as a dimer, and unlike most voltage-gated ion channels, it lacks a traditional central pore domain; instead, the voltage-sensing domain (VSD) of each monomer facilitates proton conduction via a hydrogen-bond network. Hv1 is widely expressed in various human cell types (e.g., immune cells, sperm, etc.) including tumor cells. In tumor cells, the accumulation of acidic intermediates generated by glycolysis under hypoxic conditions or ROS production leads to significant cytosolic acidification. Hv1 can remove protons from the cytosol rapidly, contributing to the adaptation of the cells to the tumor microenvironment, which may have significant consequences in tumor cell survival, proliferation, and progression. Therefore, Hv1 may be very promising not only as a tumor marker but also as a potential therapeutic target in oncology. Molecules that modulate the proton flux through Hv1 can be divided into two broad groups: inhibitors and activators. Hv1 inhibitors can be simple ions, small molecules, lipids, and peptides. In contrast, fewer Hv1 activators are known, including albumin, NH29, quercetin, and arachidonic acid. The mechanism of action of some inhibitors is well described, but not all. Hv1 modulation has profound effects on cellular physiology, especially under stress or pathological conditions, like cancer and inflammation. The therapeutic application of selective Hv1 inhibitors or activators could be a very promising strategy in the treatment of several serious diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk peptide inhibitors small molecule inhibitors Hv1 activators human Hv1
Megjelenés:	Pharmaceuticals. - 18 : 10 (2025), p. 1-15. -
További szerzők:	Mészáros Beáta (1985-) (molekuláris biológus, mikrobiológus) Szántó Gábor Tibor (1980-) (vegyész) Teshome, Russo Teklu Korpos Éva (1974-) Varga Zoltán (1969-) (biofizikus, szakfordító) Papp Ferenc (1979-) (biofizikus)
Pályázati támogatás:	University of Debrecen Program for Scientific Publication Egyéb 2024-1.2.3-HU-RIZONT- 2024-00099 Egyéb K143071 OTKA 132906 OTKA
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001-es BibID:	BIBFORM111194
035-os BibID:	(WoS)000996659300001 (Scopus)85160676201
Első szerző:	Szántó Gábor Tibor (vegyész)
Cím:	5-Chloro-2-Guanidinobenzimidazole (ClGBI) Is a Non-Selective Inhibitor of the Human HV1 Channel / Szanto Tibor G., Feher Adam, Korpos Eva, Gyöngyösi Adrienn, Kállai Judit, Mészáros Beáta, Ovari Krisztian, Lányi Árpád, Panyi Gyorgy, Varga Zoltan
Dátum:	2023
ISSN:	1424-8247
Megjegyzések:	5-chloro-2-guanidinobenzimidazole (ClGBI), a small-molecule guanidine derivative, is a known effective inhibitor of the voltage-gated proton (H+) channel (H(V)1, K-d approximate to 26 mu M) and is widely used both in ion channel research and functional biological assays. However, a comprehensive study of its ion channel selectivity determined by electrophysiological methods has not been published yet. The lack of selectivity may lead to incorrect conclusions regarding the role of hHv1 in physiological or pathophysiological responses in vitro and in vivo. We have found that ClGBI inhibits the proliferation of lymphocytes, which absolutely requires the functioning of the K(V)1.3 channel. We, therefore, tested ClGBI directly on hK(V)1.3 using a whole-cell patch clamp and found an inhibitory effect similar in magnitude to that seen on hH(V)1 (K-d approximate to 72 mu M). We then further investigated ClGBI selectivity on the hK(V)1.1, hK(V)1.4-IR, hK(V)1.5, hK(V)10.1, hK(V)11.1, hK(Ca)3.1, hNa(V)1.4, and hNa(V)1.5 channels. Our results show that, besides H(V)1 and K(V)1.3, all other off-target channels were inhibited by ClGBI, with K-d values ranging from 12 to 894 mu M. Based on our comprehensive data, ClGBI has to be considered a non-selective hH(V)1 inhibitor; thus, experiments aiming at elucidating the significance of these channels in physiological responses have to be carefully evaluated.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk ClGBI proton channel voltage-gated ion channels blocking kinetics selectivity screening
Megjelenés:	Pharmaceuticals. - 16 : 5 (2023), p. 1-15. -
További szerzők:	Fehér Ádám (1996-) (orvos, biofizikus) Korpos Éva (1974-) Gyöngyösi Adrienn (1982-) (biológus) Kállai Judit (1983-) (molekuláris biológus) Mészáros Beáta (1985-) (molekuláris biológus, mikrobiológus) Óvári Krisztián (1999-) (orvos) Lányi Árpád (1962-) (biológus, immunológus) Panyi György (1966-) (biofizikus) Varga Zoltán (1969-) (biofizikus, szakfordító)
Pályázati támogatás:	K132906 OTKA 2019-2.1.11-TÉT-2019-00059, TÉT, NKFIH Egyéb K131708 OTKA K143071 OTKA ÚNKP-22-3-II-DE-38 New National Excellence Program of the Ministry for Culture and Innovation Egyéb
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