@article{MTMT:33215047,
	title = {New ‘kids’ on the voltage‐gated proton channel block},
	url = {https://m2.mtmt.hu/api/publication/33215047},
	author = {Korpos, Éva and Papp, Ferenc},
	doi = {10.1111/febs.16670},
	journal-iso = {FEBS J},
	journal = {FEBS JOURNAL},
	volume = {290},
	unique-id = {33215047},
	issn = {1742-464X},
	year = {2023},
	eissn = {1742-4658},
	pages = {970-973},
	orcid-numbers = {Korpos, Éva/0000-0002-0438-4211}
}

@article{MTMT:33103806,
	title = {Membrane anchored IL-18 linked to constitutively active TLR4 and CD40 improves human T cell antitumor capacities for adoptive cell therapy},
	url = {https://m2.mtmt.hu/api/publication/33103806},
	author = {Blokon-Kogan, Dayana and Levi-Mann, Maya and Malka-Levy, Lior and Itzhaki, Orit and Besser, Michal J. and Shiftan, Yuval and Szöőr, Árpád and Vereb, György and Gross, Gideon and Abken, Hinrich and Weinstein-Marom, Hadas},
	doi = {10.1136/jitc-2020-001544},
	journal-iso = {J IMMUNOTHER CANCER},
	journal = {JOURNAL FOR IMMUNOTHERAPY OF CANCER},
	volume = {10},
	unique-id = {33103806},
	issn = {2051-1426},
	abstract = {Background Adoptive transfer of tumor-infiltrating lymphocytes (TILs) or blood T cells genetically redirected by an antitumor TCR or CAR induces a strong antitumor response in a proportion of patients with cancer; however, the therapeutic efficacy is often limited by rapid decline in T cell functions. Coadministering supportive cytokines frequently provokes systemic side effects preventing their broad clinical application. We recently showed that cytokines can be anchored to the cell membrane in a functional fashion and that cytokine receptor signaling can synergize with TLR4 and CD40 signaling. Here, we aimed at augmenting T cell activation by simultaneous signaling through the cytokine receptor, toll-like receptor and TNF-type receptor using IL-18, TLR4 and CD40 as prototypes. Methods Genes were expressed on electroporation of in vitro-transcribed mRNA in CD4(+) and CD8(+) T cells from healthy donors redirected against melanoma cells with an anti-melanotransferrin CAR and in TILs derived from melanoma patients. Functional assays included the activation of signaling pathways, expression of activation and differentiation markers, cytokine secretion and killing of melanoma target cells. Results To provide IL-18 costimulation to T cells in-cis while avoiding systemic effects, we genetically anchored IL-18 to the T cell membrane, either alone (memIL-18) or fused with constitutively active (ca)TLR4 and caCD40 signaling domains arranged in tandem, creating a synthetic 'all-in-one' memIL-18-TLR4-CD40 receptor. MemIL-18-TLR4-CD40, but not memIL-18, triggered strong NF-kappa B activation in cells lacking the IL-18 receptor, attesting to functionality of the TLR-CD40 moiety. While the membrane-anchored cytokine was found to act mainly in-cis, some T cell activation in-trans was also observed. The electroporated T cells exhibited spontaneous T-bet upregulation and IFN-gamma and TNF-alpha secretion. Melanoma-induced activation of CAR-T cells and TILs as manifested by cytokine secretion and cytolytic activity was substantially augmented by both constructs, with memIL-18-TLR4-CD40 exerting stronger effects than memIL-18 alone. Conclusions Linking membrane anchored IL-18 with caTLR4 and caCD40 signaling in one hybrid transmembrane protein provides simultaneous activation of three T cell costimulatory pathways through one genetically engineered membrane molecule, strongly amplifying T cell functions for adoptive T cell therapy of cancer.},
	keywords = {RECEPTORS; LYMPHOCYTES; Cytokines; immunotherapy; Adjuvants; tumor-infiltrating; Chimeric antigen; immunologic; adoptive},
	year = {2022},
	eissn = {2051-1426}
}

@article{MTMT:32886684,
	title = {Tricetin Reduces Inflammation and Acinar Cell Injury in Cerulein-Induced Acute Pancreatitis: The Role of Oxidative Stress-Induced DNA Damage Signaling},
	url = {https://m2.mtmt.hu/api/publication/32886684},
	author = {Nagy-Pénzes, Máté and Hajnády, Zoltán and Regdon, Zsolt and Demény, Máté Ágoston and Kovács, Katalin and El-Hamoly, Tarek and Maléth, József and Hegyi, Péter and Hegedűs, Csaba and Virág, László},
	doi = {10.3390/biomedicines10061371},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {10},
	unique-id = {32886684},
	year = {2022},
	eissn = {2227-9059},
	orcid-numbers = {Maléth, József/0000-0001-5768-3090; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:32851076,
	title = {Use of red, far-red, and near-infrared light in imaging of yeasts and filamentous fungi},
	url = {https://m2.mtmt.hu/api/publication/32851076},
	author = {Pócsi, István and Máthéné Szigeti, Zsuzsa and Emri, Tamás and Boczonádi, Imre and Vereb, György and Szöllősi, János},
	doi = {10.1007/s00253-022-11967-2},
	journal-iso = {APPL MICROBIOL BIOT},
	journal = {APPLIED MICROBIOLOGY AND BIOTECHNOLOGY},
	volume = {106},
	unique-id = {32851076},
	issn = {0175-7598},
	abstract = {While phototoxicity can be a useful therapeutic modality not only for eliminating malignant cells but also in treating fungal infections, mycologists aiming to observe morphological changes or molecular events in fungi, especially when long observation periods or high light fluxes are warranted, encounter problems owed to altered regulatory pathways or even cell death caused by various photosensing mechanisms. Consequently, the ever expanding repertoire of visible fluorescent protein toolboxes and high-resolution microscopy methods designed to investigate fungi in vitro and in vivo need to comply with an additional requirement: to decrease the unwanted side effects of illumination. In addition to optimizing exposure, an obvious solution is red-shifted illumination, which, however, does not come without compromises. This review summarizes the interactions of fungi with light and the various molecular biology and technology approaches developed for exploring their functions on the molecular, cellular, and in vivo microscopic levels, and outlines the progress towards reducing phototoxicity through applying far-red and near-infrared light.},
	keywords = {phototoxicity; Live-cell imaging; Time-lapse microscopy; high-resolution microscopy; Light sensing; Fluorescent proteins (FPs); Imaging toolboxes},
	year = {2022},
	eissn = {1432-0614},
	pages = {3895-3912}
}

@article{MTMT:32837061,
	title = {Epigallocatechine-3-gallate Inhibits the Adipogenesis of Human Mesenchymal Stem Cells via the Regulation of Protein Phosphatase-2A and Myosin Phosphatase},
	url = {https://m2.mtmt.hu/api/publication/32837061},
	author = {Bécsi, Bálint and Kónya, Zoltán and Boratkó, Anita and Kovács, Katalin and Erdődi, Ferenc},
	doi = {10.3390/cells11101704},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {11},
	unique-id = {32837061},
	year = {2022},
	eissn = {2073-4409}
}

@article{MTMT:32628668,
	title = {The multitargeted receptor tyrosine kinase inhibitor sunitinib induces resistance of HER2 positive breast cancer cells to trastuzumab-mediated ADCC},
	url = {https://m2.mtmt.hu/api/publication/32628668},
	author = {Guti, Eliza and Regdon, Zsolt and Sturniolo, Isotta and Kiss, Alexandra and Kovács, Katalin and Demény, Máté Ágoston and Szöőr, Árpád and Vereb, György and Szöllősi, János and Hegedűs, Csaba and Polgár, Zsuzsanna and Virág, László},
	doi = {10.1007/s00262-022-03146-z},
	journal-iso = {CANCER IMMUNOL IMMUN},
	journal = {CANCER IMMUNOLOGY IMMUNOTHERAPY},
	volume = {71},
	unique-id = {32628668},
	issn = {1432-0851},
	abstract = {Despite recent advances in the development of novel personalized therapies, breast cancer continues to challenge physicians with resistance to various advanced therapies. The anticancer action of the anti-HER2 antibody, trastuzumab, involves antibody-dependent cell-mediated cytotoxicity (ADCC) by natural killer (NK) cells. Here, we report a repurposing screen of 774 clinically used compounds on NK-cell + trastuzumab-induced killing of JIMT-1 breast cancer cells. Using a calcein-based high-content screening (HCS) assay for the image-based quantitation of ADCC that we have developed and optimized for this purpose, we have found that the multitargeted tyrosine kinase inhibitor sunitinib inhibits ADCC in this model. The cytoprotective effect of sunitinib was also confirmed with two other assays (lactate dehydrogenase release, and electric cell substrate impedance sensing, ECIS). The drug suppressed NK cell activation as indicated by reduced granzyme B deposition on to the target cells and inhibition of interferon-γ production by the NK cells. Moreover, sunitinib induced downregulation of HER2 on the target cells' surface, changed the morphology and increased adherence of the target cells. Moreover, sunitinib also triggered the autophagy pathway (speckled LC3b) as an additional potential underlying mechanism of the cytoprotective effect of the drug. Sunitinib-induced ADCC resistance has been confirmed in a 3D tumor model revealing the prevention of apoptotic cell death (Annexin V staining) in JIMT-1 spheroids co-incubated with NK cells and trastuzumab. In summary, our HCS assay may be suitable for the facile identification of ADCC boosting compounds. Our data urge caution concerning potential combinations of ADCC-based immunotherapies and sunitinib.},
	keywords = {breast cancer; natural killer cell; trastuzumab; sunitinib; antibody-dependent cell mediated cytotoxicity (ADCC); Herceptin},
	year = {2022},
	eissn = {0340-7004},
	pages = {2151-2168}
}

@{MTMT:32852451,
	title = {Expression of indoleamine 2,3-dioxygenase (IDO) and PTEN in human renal carcinoma},
	url = {https://m2.mtmt.hu/api/publication/32852451},
	author = {Kónya, Gábor and Szabó, Zsuzsanna and Király, József and Dobos, Nikoletta and Zsebik, Barbara and Szegedi, Krisztián and Halmos, Gábor},
	booktitle = {Medical Conference for PhD Students and Experts of Clinical Sciences 2021},
	unique-id = {32852451},
	year = {2021},
	pages = {103}
}

@article{MTMT:32733912,
	title = {The presence of Tks4 augments tumor progression},
	url = {https://m2.mtmt.hu/api/publication/32733912},
	author = {Gyongyosi, Adrienn and Boldizsar, Eszter and Kállai, Judit and Czuczku, Daniel and Alala, Siham and Laoui, Damya and Van Ginderachter, Jo A. and Lanyi, Arpad},
	journal-iso = {EUR J IMMUNOL},
	journal = {EUROPEAN JOURNAL OF IMMUNOLOGY},
	volume = {51},
	unique-id = {32733912},
	issn = {0014-2980},
	keywords = {cancer immunology; myeloid derived suppressor cells; in vivo tumor models},
	year = {2021},
	eissn = {1521-4141},
	pages = {324-324}
}

@article{MTMT:32512952,
	title = {Isocyanide Substitution in Acridine Orange Shifts DNA Damage-Mediated Phototoxicity to Permeabilization of the Lysosomal Membrane in Cancer Cells},
	url = {https://m2.mtmt.hu/api/publication/32512952},
	author = {Bankó, Csaba and Nagy, Zsolt László and Nagy, Miklós and Szemán-Nagy, Gábor and Rebenku, István and Imre, László and Tiba, Attila and Hajdu, András and Szöllősi, János and Kéki, Sándor and Bacsó, Zsolt},
	doi = {10.3390/cancers13225652},
	journal-iso = {CANCERS},
	journal = {CANCERS},
	volume = {13},
	unique-id = {32512952},
	year = {2021},
	eissn = {2072-6694},
	orcid-numbers = {Nagy, Miklós/0000-0002-3484-2244; Szemán-Nagy, Gábor/0000-0003-1906-0188}
}

@article{MTMT:32498912,
	title = {Oxidative stress-induced DNA damage signaling: the role of poly(ADP-ribose) polymerase 1},
	url = {https://m2.mtmt.hu/api/publication/32498912},
	author = {Regdon, Zsolt and Demény, Máté Ágoston and Hegedűs, Csaba and Kiss, Alexandra and Szabo, E. and Virág, László},
	journal-iso = {FEBS OPEN BIO},
	journal = {FEBS OPEN BIO},
	volume = {11},
	unique-id = {32498912},
	issn = {2211-5463},
	year = {2021},
	eissn = {2211-5463},
	pages = {61-61}
}