@article{MTMT:34836717,
	title = {Microcystin-LR, a cyanotoxin, modulates division of higher plant chloroplasts through protein phosphatase inhibition and affects cyanobacterial division},
	url = {https://m2.mtmt.hu/api/publication/34836717},
	author = {Máthé, Csaba and Bóka, Károly and Kónya, Zoltán and Erdődi, Ferenc and Vasas, Gábor and Freytag, Csongor and Garda, Tamás},
	doi = {10.1016/j.chemosphere.2024.142125},
	journal-iso = {CHEMOSPHERE},
	journal = {CHEMOSPHERE},
	volume = {358},
	unique-id = {34836717},
	issn = {0045-6535},
	keywords = {PROTEIN PHOSPHATASE; microcystin-LR; Arabidopsis.; chloroplast division/fission},
	year = {2024},
	eissn = {1879-1298},
	orcid-numbers = {Bóka, Károly/0000-0002-1324-3592; Freytag, Csongor/0000-0002-3356-4182}
}

@article{MTMT:34820104,
	title = {Quantifying antibody-dependent cellular cytotoxicity in a tumor spheroid model : application for drug discovery},
	url = {https://m2.mtmt.hu/api/publication/34820104},
	author = {Isotta, Sturniolo and Csongor, Váróczy and Ákos, Máté Bede and Hegedűs, Csaba and Demény, Máté Ágoston and Virág, László},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	unique-id = {34820104},
	issn = {1940-087X},
	year = {2024},
	eissn = {1940-087X}
}

@article{MTMT:34817464,
	title = {Specific and shared biological functions of PARP2 – is PARP2 really a lil’ brother of PARP1?},
	url = {https://m2.mtmt.hu/api/publication/34817464},
	author = {Szántó, Magdolna and Yélamos, J and Bay, Péter},
	journal-iso = {EXPERT REV MOL MED},
	journal = {EXPERT REVIEWS IN MOLECULAR MEDICINE},
	volume = {26},
	unique-id = {34817464},
	issn = {1462-3994},
	year = {2024},
	eissn = {1462-3994},
	pages = {1-21}
}

@article{MTMT:34813914,
	title = {Synthesis, in silico and kinetics evaluation of N-(beta-D-glucopyranosyl)-2-arylimidazole-4(5)-carboxamides and N-(beta-D-glucopyranosyl)-4(5)-arylimidazole-2-carboxamides as glycogen phosphorylase inhibitors},
	url = {https://m2.mtmt.hu/api/publication/34813914},
	author = {Homolya, Levente and Mathomes, Rachel T. and Fodor-Varga, Luca Anna and Docsa, Tibor and Juhász, László and Hayes, Joseph M. and Somsák, László},
	doi = {10.3390/ijms25094591},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34813914},
	issn = {1661-6596},
	abstract = {Recently studied N-(β-D-glucopyranosyl)-3-aryl-1,2,4-triazole-5-carboxamides have proven to be low micromolar inhibitors of glycogen phosphorylase (GP), a validated target for the treatment of type 2 diabetes mellitus. Since in other settings, the bioisosteric replacement of the 1,2,4-triazole moiety with imidazole resulted in significantly more efficient GP inhibitors, in silico calculations using Glide molecular docking along with unbound state DFT calculations were performed on N-(β-Dglucopyranosyl)-arylimidazole-carboxamides, revealing their potential for strong GP inhibition. The syntheses of the target compounds involved the formation of an amide bond between per-O-acetylated β-D-glucopyranosylamine and the corresponding arylimidazole-carboxylic acids. Kinetics experiments on rabbit muscle GPb revealed low micromolar inhibitors, with the best inhibition constants (Kis) of ~3–4 µM obtained for 1- and 2-naphthyl-substituted N-(β-D-glucopyranosyl)-imidazolecarboxamides, 2b–c. The predicted protein–ligand interactions responsible for the observed potencies are discussed and will facilitate the structure-based design of other inhibitors targeting this important therapeutic target. Meanwhile, the importance of the careful consideration of ligand tautomeric states in binding calculations is highlighted, with the usefulness of DFT calculations in this regard proposed.},
	keywords = {Glycogen phosphorylase inhibitor; Tautomers; type 2 diabetes; glucose analogues},
	year = {2024},
	eissn = {1422-0067},
	pages = {1-21},
	orcid-numbers = {Juhász, László/0000-0002-7462-7944; Somsák, László/0000-0002-9103-9845}
}

@article{MTMT:34754751,
	title = {PARP14 contributes to the development of the tumor-associated macrophage phenotype},
	url = {https://m2.mtmt.hu/api/publication/34754751},
	author = {Sturniolo, I and Váróczy, Cs and Regdon, Zsolt and Mázló, A and Muzsai, Sz and Bácsi, A and Intili, G and Hegedűs, Csaba and Boothby, MR and Holechek, J and Ferraris, D and Schüler, H and Virág, László},
	doi = {10.3390/ijms25073601},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34754751},
	issn = {1661-6596},
	year = {2024},
	eissn = {1422-0067},
	pages = {1-21}
}

@article{MTMT:34747207,
	title = {Ünnepelt a Debreceni Egyetem Orvosi Vegytani Intézete: 70 éves Dombrádi Viktor és Erdődi Ferenc},
	url = {https://m2.mtmt.hu/api/publication/34747207},
	author = {Lontay, Beáta},
	journal-iso = {BIOKÉMIA},
	journal = {BIOKÉMIA: A MAGYAR BIOKÉMIAI EGYESÜLET FOLYÓIRATA},
	volume = {XLVIII},
	unique-id = {34747207},
	issn = {0133-8455},
	year = {2024},
	eissn = {2060-8152},
	pages = {96-100}
}

@article{MTMT:34738061,
	title = {Stable knockdown of Drp1 improves retinoic acid-BDNF-induced neuronal differentiation through global transcriptomic changes and results in reduced phosphorylation of ERK1/2 independently of DUSP1 and 6},
	url = {https://m2.mtmt.hu/api/publication/34738061},
	author = {Ghani, Marvi and Zohar, Peleg and Ujlaki, Gyula and Tóth, Melinda and Amsalu, Hailemariam and Póliska, Szilárd and Tar, Krisztina},
	doi = {10.3389/fcell.2024.1342741},
	journal-iso = {FRONT CELL DEV BIOL},
	journal = {FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY},
	volume = {12},
	unique-id = {34738061},
	issn = {2296-634X},
	abstract = {Background: Dynamin-related protein Drp1 —a major mitochondrial fission protein— is widely distributed in the central nervous system and plays a crucial role in regulating mitochondrial dynamics, specifically mitochondrial fission and the organelle's shaping. Upregulated Drp1 function may contribute to the pathological progression of neurodegenerative diseases by dysregulating mitochondrial fission/ fusion. The study aims to investigate the effects of Drp1 on retinoic acid-BDNF-induced (RA-BDNF) neuronal differentiation and mitochondrial network reorganization in SH-SY5Y neuroblastoma cells.},
	year = {2024},
	eissn = {2296-634X},
	pages = {1-25}
}

@article{MTMT:34573513,
	title = {PP2A Affects Angiogenesis via Its Interaction with a Novel Phosphorylation Site of TSP1},
	url = {https://m2.mtmt.hu/api/publication/34573513},
	author = {Thalwieser, Zsófia and Fonódi, Márton and Király, Nikolett and Csortos, Csilla and Boratkó, Anita},
	doi = {10.3390/ijms25031844},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34573513},
	issn = {1661-6596},
	abstract = {Alterations in angiogenic properties play a pivotal role in the manifestation and onset of various pathologies, including vascular diseases and cancer. Thrombospondin-1 (TSP1) protein is one of the master regulators of angiogenesis. This study unveils a novel aspect of TSP1 regulation through reversible phosphorylation. The silencing of the B55α regulatory subunit of protein phosphatase 2A (PP2A) in endothelial cells led to a significant decrease in TSP1 expression. Direct interaction between TSP1 and PP2A-B55α was confirmed via various methods. Truncated TSP1 constructs were employed to identify the phosphorylation site and the responsible kinase, ultimately pinpointing PKC as the enzyme phosphorylating TSP1 on Ser93. The biological effects of B55α–TSP1 interaction were also analyzed. B55α silencing not only counteracted the increase in TSP1 expression during wound closure but also prolonged wound closure time. Although B55α silenced cells initiated tube-like structures earlier than control cells, their spheroid formation was disrupted, leading to disintegration. Cells transfected with phosphomimic TSP1 S93D exhibited smaller spheroids and reduced effectiveness in tube formation, revealing insights into the effects of TSP1 phosphorylation on angiogenic properties. In this paper, we introduce a new regulatory mechanism of angiogenesis by reversible phosphorylation on TSP1 S93 by PKC and PP2A B55α.},
	year = {2024},
	eissn = {1422-0067},
	pages = {1844}
}

@article{MTMT:34483936,
	title = {Cell-free ascites from ovarian cancer patients induces Warburg metabolism and cell proliferation through TGFbeta-ERK signalling},
	url = {https://m2.mtmt.hu/api/publication/34483936},
	author = {Szeőcs, Dóra and Vida, Beáta and Petővári, Gábor and Póliska, Szilárd and Janka, Eszter Anna and Sipos, Adrienn and Uray (Davis), Karen L. and Sebestyén, Anna and Krasznai, Zoárd Tibor and Bay, Péter},
	doi = {10.1007/s11357-023-01056-1},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	unique-id = {34483936},
	issn = {2509-2715},
	abstract = {Ascites plays a key role in supporting the metastatic potential of ovarian cancer cells. Shear stress and carry-over of cancer cells by ascites flow support carcinogenesis and metastasis formation. In addition, soluble factors may participate in the procarcinogenic effects of ascites in ovarian cancer. This study aimed to determine the biological effects of cell-free ascites on carcinogenesis in ovarian cancer cells. Cell-free ascites from ovarian cancer patients (ASC) non-selectively induced cell proliferation in multiple models of ovarian cancer and untransformed primary human dermal fibroblasts. Furthermore, ASC induced a Warburg-type rearrangement of cellular metabolism in A2780 ovarian cancer cells characterized by increases in cellular oxygen consumption and glycolytic flux; increases in glycolytic flux were dominant. ASC induced mitochondrial uncoupling and fundamentally reduced fatty acid oxidation. Ascites-elicited effects were uniform among ascites specimens. ASC-elicited transcriptomic changes in A2780 ovarian cancer cells included induction of the TGF beta-ERK/MEK pathway, which plays a key role in inducing cell proliferation and oncometabolism. ASC-induced gene expression changes, as well as the overexpression of members of the TGF beta signaling system, were associated with poor survival in ovarian cancer patients. We provided evidence that the activation of the autocrine/paracrine of TGF beta signaling system may be present in bladder urothelial carcinoma and stomach adenocarcinoma. Database analysis suggests that the TGF beta system may feed forward bladder urothelial carcinoma and stomach adenocarcinoma. Soluble components of ASC support the progression of ovarian cancer. These results suggest that reducing ascites production may play an essential role in the treatment of ovarian cancer by inhibiting the progression and reducing the severity of the disease.},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Petővári, Gábor/0000-0002-1957-2864; Janka, Eszter Anna/0000-0003-0724-5281; Sebestyén, Anna/0000-0001-8814-4794}
}

@article{MTMT:34148390,
	title = {Distinct subsets of anti-pulmonary autoantibodies correlate with disease severity and survival in severe COVID-19 patients},
	url = {https://m2.mtmt.hu/api/publication/34148390},
	author = {Tóth, Emese and Fagyas, Miklós and Nagy, Béla and Siket, Ivetta Mányiné and Szőke, Blanka and Mártha, Lilla and Mahdi, Mohamed and Erdősi, Gábor and Pólik, Zsófia and Kappelmayer, János and Papp, Zoltán and Borbély, Attila and Szabó, Tamás and Balla, József and Balla, György and Bácsi, Attila and Szekanecz, Zoltán and Bay, Péter and Tóth, Attila},
	doi = {10.1007/s11357-023-00887-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34148390},
	issn = {2509-2715},
	abstract = {Autoantibodies targeting the lung tissue were identified in severe COVID-19 patients in this retrospective study. Fifty-three percent of 104 patients developed anti-pulmonary antibodies, the majority of which were IgM class, suggesting that they developed upon infection with SARS-CoV-2. Anti-pulmonary antibodies correlated with worse pulmonary function and a higher risk of multiorgan failure that was further aggravated if 3 or more autoantibody clones were simultaneously present (multi-producers). Multi-producer patients were older than the patients with less or no autoantibodies. One of the identified autoantibodies (targeting a pulmonary protein of ~ 50 kDa) associated with worse clinical outcomes, including mortality. In summary, severe COVID-19 is associated with the development of lung-specific autoantibodies, which may worsen the clinical outcome. Tissue proteome-wide tests, such as the ones applied here, can be used to detect autoimmunity in the post-COVID state to identify the cause of symptoms and to reveal a new target for treatment.},
	year = {2024},
	eissn = {2509-2723},
	pages = {1561-1574}
}