@article{MTMT:36374125,
	title = {Developing an ex vivo human cornea model for discovering the cellular interactions in simple limbal epithelial transplantation},
	url = {https://m2.mtmt.hu/api/publication/36374125},
	author = {Kemenes, Gréta and Rebenku, István and Vereb, György and Takács, Lili},
	journal-iso = {INVEST OPHTH VIS SCI},
	journal = {INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE},
	volume = {66},
	unique-id = {36374125},
	issn = {0146-0404},
	year = {2025},
	eissn = {1552-5783},
	pages = {1042}
}

@article{MTMT:33124821,
	title = {The hEag1 K+ Channel Inhibitor Astemizole Stimulates Ca2+ Deposition in SaOS-2 and MG-63 Osteosarcoma Cultures},
	url = {https://m2.mtmt.hu/api/publication/33124821},
	author = {Mészáros, Beáta and Csóti, Ágota and Szántó, Gábor Tibor and Telek, Andrea and Kovács, Katalin and Tóth, Ágnes and Volkó, Julianna and Panyi, György},
	doi = {10.3390/ijms231810533},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33124821},
	issn = {1661-6596},
	abstract = {The hEag1 (Kv10.1) K+ channel is normally found in the brain, but it is ectopically expressed in tumor cells, including osteosarcoma. Based on the pivotal role of ion channels in osteogenesis, we tested whether pharmacological modulation of hEag1 may affect osteogenic differentiation of osteosarcoma cell lines. Using molecular biology (RT-PCR), electrophysiology (patch-clamp) and pharmacology (astemizole sensitivity, IC50 = 0.135 mu M) we demonstrated that SaOS-2 osteosarcoma cells also express hEag1 channels. SaOS-2 cells also express to KCa1.1 K+ channels as shown by mRNA expression and paxilline sensitivity of the current. The inhibition of hEag1 (2 mu M astemizole) or KCa1.1 (1 mM TEA) alone did not induce Ca2+ deposition in SaOS-2 cultures, however, these inhibitors, at identical concentrations, increased Ca2+ deposition evoked by the classical or pathological (inorganic phosphate, Pi) induction pathway without causing cytotoxicity, as reported by three completer assays (LDH release, MTT assay and SRB protein assay). We observed a similar effect of astemizole on Ca2+ deposition in MG-63 osteosarcoma cultures as well. We propose that the increase in the osteogenic stimuli-induced mineral matrix formation of osteosarcoma cell lines by inhibiting hEag1 may be a useful tool to drive terminal differentiation of osteosarcoma.},
	keywords = {ASSAY; ACTIVATION; GATED POTASSIUM CHANNELS; CELL-PROLIFERATION; ether; VASCULAR CALCIFICATION; Biochemistry & Molecular Biology; Osteogenic differentiation; Osteoblastic differentiation; Kv10; BONE-CELLS; hEag1 potassium channel; SaOS-2 osteosarcoma cells; Ca2+ deposition},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Panyi, György/0000-0001-6227-3301}
}

@article{MTMT:30323488,
	title = {Minimum degree of overlap between IL-9R and IL-2R on human T lymphoma cells: A quantitative CLSM and FRET analysis},
	url = {https://m2.mtmt.hu/api/publication/30323488},
	author = {Nizsalóczki, Enikő and Nagy, Péter and Mocsár, Gábor and Szabó, Ágnes Tímea and Csomós, István and Waldmann, Thomas A. and Vámosi, György and Mátyus, László and Bodnár, Andrea},
	doi = {10.1002/cyto.a.23634},
	journal-iso = {CYTOM PART A},
	journal = {CYTOMETRY PART A},
	volume = {93},
	unique-id = {30323488},
	issn = {1552-4922},
	abstract = {The heterodimeric receptor complex of IL-9 consists of the cytokine-specific alpha-subunit and the common gamma(c)-chain shared with other cytokines, including IL-2, a central regulator of T cell function. We have shown previously the bipartite spatial relationship of IL-9 and IL-2 receptors at the surface of human T lymphoma cells: in addition to common clusters, expression of the two receptor kinds could also be observed in segregated membrane areas. Here we analyzed further the mutual cell surface organization of IL-9 and IL-2 receptors. Complementing Pearson correlation data with co-occurrence analysis of confocal microscopic images revealed that a minimum degree of IL-9R/IL-2R co-localization exists at the cell surface regardless of the overall spatial correlation of the two receptor kinds. Moreover, our FRET experiments demonstrated molecular scale assemblies of the elements of the IL-9/IL-2R system. Binding of IL-9 altered the structure and/or composition of these clusters. It is hypothesized, that by sequestering receptor subunits in common membrane areas, the overlapping domains of IL-9R and IL-2R provide a platform enabling both the formation of the appropriate receptor complex as well as subunit sharing between related cytokines. (c) 2018 International Society for Advancement of Cytometry},
	keywords = {Fluorescence Resonance Energy Transfer; confocal microscopy; IL-9 and-2 receptors; co-localization of membrane proteins; human T lymphoma cells; Pearson correlation analysis; co-occurrence analysis; Manders coefficient},
	year = {2018},
	eissn = {1552-4930},
	pages = {1106-1117},
	orcid-numbers = {Nagy, Péter/0000-0002-7466-805X}
}

@article{MTMT:2439654,
	title = {V-ATPase inhibition overcomes trastuzumab resistance in breast cancer.},
	url = {https://m2.mtmt.hu/api/publication/2439654},
	author = {von Schwarzenberg, K and Lajtos, Tamás and Simon, László and Muller, R and Vereb, György and Vollmar, AM},
	doi = {10.1016/j.molonc.2013.08.011},
	journal-iso = {MOL ONCOL},
	journal = {MOLECULAR ONCOLOGY},
	volume = {8},
	unique-id = {2439654},
	issn = {1574-7891},
	abstract = {The HER2 oncogene targeting drug trastuzumab shows remarkable efficacy in patients overexpressing HER2. However acquired or primary resistance develops in most of the treated patients why alternative treatment strategies are strongly needed. As endosomal sorting and recycling are crucial steps for HER2 activity and the vacuolar H+-ATPase (V-ATPase) is an important regulator of endocytotic trafficking, we proposed that targeting V-ATPase opens a new therapeutic strategy against trastuzumab-resistant tumor cells in vitro and in vivo. V-ATPase inhibition with archazolid, a novel inhibitor of myxobacterial origin, results in growth inhibition, apoptosis and impaired HER2 pro-survival signaling of the trastuzumab-resistant cell line JIMT-1. This is accompanied by a decreased expression on the plasma membrane and accumulation of HER2 in the cytosol, where it colocalizes with endosomes, lysosomes and autophagosomes. Importantly, microscopic analysis of JIMT-1 xenograft tumor tissue of archazolid treated mice confirms the defect in HER2-recycling which leads to reduced tumor growth. These results suggest that V-ATPase inhibition by archazolid induces apoptosis and inhibits growth of trastuzumab-resistant tumor cells by retaining HER2 in dysfunctional vesicles of the recycling pathway and consequently abrogates HER2-signaling in vitro as well as in vivo. V-ATPase inhibition is thus suggested as a promising strategy for treatment of trastuzumab-resistant tumors.},
	year = {2014},
	eissn = {1878-0261},
	pages = {9-19},
	orcid-numbers = {Simon, László/0000-0003-4321-8539}
}

@article{MTMT:2239256,
	title = {Analysis of the K+ current in human CD4+ T lymphocytes in hypercholesterolemic state},
	url = {https://m2.mtmt.hu/api/publication/2239256},
	author = {Somodi, Sándor and Balajthy, András and Szilágyi, Orsolya and Pethő, Zoltán Dénes and Harangi, Mariann and Paragh, György and Panyi, György and Hajdu, Péter Béla},
	doi = {10.1016/j.cellimm.2013.01.004},
	journal-iso = {CELL IMMUNOL},
	journal = {CELLULAR IMMUNOLOGY},
	volume = {281},
	unique-id = {2239256},
	issn = {0008-8749},
	abstract = {Atherosclerosis involves immune mechanisms: T lymphocytes are found in atherosclerotic plaques, suggesting their activation during atherogenesis. The predominant voltage-gated potassium channel of T cells, Kv1.3 is a key regulator of the Ca2+-dependent activation pathway. In the present experiments we studied the proliferation capacity and functional changes of Kv1.3 channels in T cells from healthy and hypercholestaeremic patients.By means of CFSE-assay (carboxyfluorescein succinimidyl ester) we showed that spontaneous activation rate of lymphocytes in hypercholesterolemia was elevated and the antiCD3/antiCD28 co-stimulation was less effective as compared to the healthy group. Using whole-cell patch-clamping we obtained that the activation and deactivation kinetics of Kv1.3 channels were faster in hypercholesterolemic state but no change in other parameters of Kv1.3 were found (inactivation kinetics, steady-state activation, expression level). We suppose that incorporation of oxLDL species via its raft-rupturing effect can modify proliferative rate of T cells as well as the gating of Kv1.3 channels. © 2013 Elsevier Inc.},
	keywords = {PROLIFERATION; cholesterol; T lymphocyte; Kv1.3},
	year = {2013},
	eissn = {1090-2163},
	pages = {20-26},
	orcid-numbers = {Somodi, Sándor/0000-0002-3615-2300; Pethő, Zoltán Dénes/0000-0001-7057-4761; Panyi, György/0000-0001-6227-3301}
}

@article{MTMT:2273474,
	title = {The role of PSD-95 in the rearrangement of Kv1.3 channels to the immunological synapse},
	url = {https://m2.mtmt.hu/api/publication/2273474},
	author = {Szilágyi, Orsolya and Boratkó, Anita and Panyi, György and Hajdu, Péter Béla},
	doi = {10.1007/s00424-013-1256-6},
	journal-iso = {PFLUG ARCH EUR J PHY},
	journal = {PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY},
	volume = {465},
	unique-id = {2273474},
	issn = {0031-6768},
	year = {2013},
	eissn = {1432-2013},
	pages = {1341-1353},
	orcid-numbers = {Panyi, György/0000-0001-6227-3301}
}

@article{MTMT:2407334,
	title = {The COMPASS Subunit Spp1 Links Histone Methylation to Initiation of Meiotic Recombination},
	url = {https://m2.mtmt.hu/api/publication/2407334},
	author = {Acquaviva, L and Székvölgyi, Lóránt and Dichtl, B and Dichtl, BS and Saint, Andre CD and Nicolas, A and Geli, V},
	doi = {10.1126/science.1225739},
	journal-iso = {SCIENCE},
	journal = {SCIENCE},
	volume = {339},
	unique-id = {2407334},
	issn = {0036-8075},
	year = {2013},
	eissn = {1095-9203},
	pages = {215-218}
}

@misc{MTMT:33614989,
	title = {Locked-open activation gate prevents the recovery of Shaker-IR K+ channels from slow inactivation},
	url = {https://m2.mtmt.hu/api/publication/33614989},
	author = {Panyi, György},
	unique-id = {33614989},
	year = {2013},
	orcid-numbers = {Panyi, György/0000-0001-6227-3301}
}

@article{MTMT:1762844,
	title = {Bare lymphocyte syndrome: An opportunity to discover our immune system.},
	url = {https://m2.mtmt.hu/api/publication/1762844},
	author = {Shrestha, D and Szöllősi, János and Jenei, Attila},
	doi = {10.1016/j.imlet.2011.10.007},
	journal-iso = {IMMUNOL LETT},
	journal = {IMMUNOLOGY LETTERS},
	volume = {141},
	unique-id = {1762844},
	issn = {0165-2478},
	abstract = {Bare lymphocyte syndrome (BLS) is a rare immunodeficiency disorder manifested by the partial or complete disappearance of major histocompatibility complex (MHC) proteins from the surface of the cells. Based on this specific feature, it is categorized into three different types depending on which type of MHC protein is affected. These proteins are mainly involved in generating the effective immune responses by differentiating 'self' from 'non-self' antigens through a process referred to as antigen presentation. Investigations on BLS have immensely contributed to our understanding of the transcriptional regulation of these molecules and have led to the discovery of several important proteins of the antigen presentation pathway. Reviews on this subject consistently project type II BLS, MHC II deficiency as BLS syndrome, although literatures' document cases of other types of BLS too. Therefore, in this article, we have assembled information on the BLS syndrome to produce a systematic narration while emphasizing the importance of BLS system in studying various aspects of immune biology.},
	year = {2012},
	eissn = {1879-0542},
	pages = {147-157}
}

@article{MTMT:1766979,
	title = {Coating conditions matter to collagen matrix formation regarding von Willebrand factor and platelet binding. Collagen matrix matters to VWF and platelet binding},
	url = {https://m2.mtmt.hu/api/publication/1766979},
	author = {Shlomit, Mendelboum Raviv and Szekeres-Csiki, Katalin and Jenei, Attila and Janos, Nagy and Boris, Shenkman and Naphtali, Savion and Hársfalvi, Jolán},
	doi = {10.1016/j.thromres.2011.09.030},
	journal-iso = {THROMB RES},
	journal = {THROMBOSIS RESEARCH},
	volume = {129},
	unique-id = {1766979},
	issn = {0049-3848},
	year = {2012},
	eissn = {1879-2472},
	pages = {25-29},
	orcid-numbers = {Hársfalvi, Jolán/0000-0001-9940-4846}
}