@article{MTMT:34767195,
	title = {Pharmacological Activation of Piezo1 Channels Enhances Astrocyte–Neuron Communication via NMDA Receptors in the Murine Neocortex},
	url = {https://m2.mtmt.hu/api/publication/34767195},
	author = {Csemer , Andrea and Sokvári, Cintia and Maamrah, Baneen and Szabó, László and Korpás, Kristóf Levente and Deák-Pocsai, Krisztina and Pál, Balázs Zoltán},
	doi = {10.3390/ijms25073994},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34767195},
	issn = {1661-6596},
	abstract = {The Piezo1 mechanosensitive ion channel is abundant on several elements of the central nervous system including astrocytes. It has been already demonstrated that activation of these channels is able to elicit calcium waves on astrocytes, which contributes to the release of gliotransmitters. Astrocyte- and N-methyl-D-aspartate (NMDA) receptor-dependent slow inward currents (SICs) are hallmarks of astrocyte–neuron communication. These currents are triggered by glutamate released as gliotransmitter, which in turn activates neuronal NMDA receptors responsible for this inward current having slower kinetics than any synaptic events. In this project, we aimed to investigate whether Piezo1 activation and inhibition is able to alter spontaneous SIC activity of murine neocortical pyramidal neurons. When the Piezo1 opener Yoda1 was applied, the SIC frequency and the charge transfer by these events in a minute time was significantly increased. These changes were prevented by treating the preparations with the NMDA receptor inhibitor D-AP5. Furthermore, Yoda1 did not alter the spontaneous EPSC frequency and amplitude when SICs were absent. The Piezo1 inhibitor Dooku1 effectively reverted the actions of Yoda1 and decreased the rise time of SICs when applied alone. In conclusion, activation of Piezo1 channels is able to alter astrocyte–neuron communication. Via enhancement of SIC activity, astrocytic Piezo1 channels have the capacity to determine neuronal excitability.},
	keywords = {glutamate; Slow inward current; NMDA receptor; ASTROCYTE; neocortex; Pyramidal cell; PIEZO1; Yoda1; Dooku1},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Korpás, Kristóf Levente/0009-0005-4440-2460}
}

@article{MTMT:34762667,
	title = {Universal CAR T cells targeted to HER2 with a biotin-trastuzumab soluble linker penetrate spheroids and large tumor xenografts that are inherently resistant to trastuzumab mediated ADCC},
	url = {https://m2.mtmt.hu/api/publication/34762667},
	author = {Nagy, Lőrinc and Mezősi-Csaplár, Marianna and Rebenku, István and Vereb, György and Szöőr, Árpád},
	doi = {10.3389/fimmu.2024.1365172},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {15},
	unique-id = {34762667},
	issn = {1664-3224},
	abstract = {CAR T cell therapies face challenges in combating solid tumors due to their single-target approach, which becomes ineffective if the targeted antigen is absent or lost. Universal CAR T cells (UniCAR Ts) provide a promising solution by utilizing molecular tags (linkers), such as biotin conjugated to monoclonal antibodies, enabling them to target a variety of tumor antigens. Recently, we showed that conventional CAR T cells could penetrate the extracellular matrix (ECM) of ADCC-resistant tumors, which forms a barrier to therapeutic antibodies. This finding led us to investigate whether UniCAR T cells, targeted by soluble antibody-derived linkers, could similarly tackle ADCC-resistant tumors where ECM restricts antibody penetration. We engineered UniCAR T cells by incorporating a biotin-binding monomeric streptavidin 2 (mSA2) domain for targeting HER2 via biotinylated trastuzumab (BT). The activation and cytotoxicity of UniCAR T cells in the presence or absence of BT were evaluated in conventional immunoassays. A 3D spheroid coculture was set up to test the capability of UniCAR Ts to access ECM-masked HER2 + cells. For in vivo analysis, we utilized a HER2 + xenograft model in which intravenously administered UniCAR T cells were supplemented with intraperitoneal BT treatments. In vitro , BT-guided UniCAR T cells showed effective activation and distinct anti-tumor response. Upon target recognition, IFNγ secretion correlated with BT concentration. In the presence of BT, UniCAR T cells effectively penetrated HER2 + spheroids and induced cell death in their core regions. In vivo , upon intravenous administration of UniCAR Ts, circulating BT linkers immediately engaged the mSA2 domain and directed effector cells to the HER2 + tumors. However, these co-treated mice died early, possibly due to the lung infiltration of UniCAR T cells that could recognize both native biotin and HER2. Our results suggest that UniCAR T cells guided with soluble linkers present a viable alternative to conventional CAR T cells, especially for patients resistant to antibody therapy and those with solid tumors exhibiting high antigenic variability. Critical to their success, however, is the choice of an appropriate binding domain for the CAR and the corresponding soluble linker, ensuring both efficacy and safety in therapeutic applications.},
	year = {2024},
	eissn = {1664-3224},
	pages = {1664-3224},
	orcid-numbers = {Nagy, Lőrinc/0000-0001-5278-1898}
}

@mastersthesis{MTMT:34743201,
	title = {A citoszkeletális Szeptin7 fehérje szerepének vizsgálata C2C12 sejtkultúrákon},
	url = {https://m2.mtmt.hu/api/publication/34743201},
	author = {Ráduly, Zsolt},
	publisher = {University Debrecen Doctoral School of Molecular Medicine!},
	unique-id = {34743201},
	abstract = {A vázizomsérülések során a gyors regenerációnak kiemelt egészségügyi, szociális és gazdasági szerepe van. Az elmúlt 50 év kutatásai rávilágítottak a tényre, hogy az aktin, mikrotubulusok és az intermedier filamentumok mellett a szeptinek csoportja is kiemelkedő szereppel bír a citoszkeleton felépítésében és szabályozásában. A szeptinek egymással változatos módon képesek kölcsönhatásokat létrehozni, ezzel olyan hetero-oligomereket és makromolekuláris komplexeket képezve, melyek a sejtosztódás, differenciálódás, migráció, immunválaszok és áttétképződések folyamataiban szerepet játszhatnak. Jelen dolgozatban a Szeptin7 fehérje szerepe kerül ismertetésre in vitro, C2C12 sejteken mért adatok felhasználásával. Eredményeink alapján kijelenthetjük, hogy a különböző szeptin fehérjék a C2C12 sejtek különböző fejlődési állapotaiban eltérően fejeződnek ki. Bebizonyítottuk, hogy Szeptin7 nélkül a sejtek nem képesek osztódni és a Szeptin7 elengedhetetlen a miotubulusok képződéséhez. Kimutattuk, hogy a Szeptin7 a citoszkeleton szerves részeként hozzájárul a sejtalak meghatározásához a mioblasztokban. Méréseink alapján feltételezzük, hogy a Szeptin7 hatással van a sejtek mitokondriális rendszerére is. Bizonyítékot szolgáltattunk arra, hogy a Szeptin7 filamentumok átrendeződnek a mioblasztok migrációja során. A Szeptin7 expressziójának downregulációja a migráció paramétereinek megváltozását eredményezte. A Szeptin7 különleges szerepét a mioblasztok migrációjában a forklórfenuron (FCF) kezelés is igazolja. Az FCF dózisfüggő módon gátolja a C2C12 sejtek proliferációját és vélhetően az FCF kezelés hatására a szeptin filamentumok dinamikus átrendeződése is gátolt, ezáltal a migrációs paraméterek is megváltoztak. Összességében a Szeptin7 fehérje alapvető szerepet játszik a mioblasztok proliferációs, differenciációs és migrációs folyamataiban, melyek kulcsfontosságú események a funkcionális vázizomrostok fejlődési és regenerációs szakaszaiban. 
		
		Rapid recovery from musculoskeletal injuries is a priority in health, social and economic terms. Research over the past 50 years has highlighted the fact that, in addition to actin, microtubules and intermediate filaments, septins play a prominent role in the assembly and regulation of the cytoskeleton. Septins can interact with each other in a variety of ways, forming hetero-oligomers and macromolecular complexes that may be involved in processes of cell division, differentiation, migration, immune responses and metastasis. In this thesis, the role of the Septin7 protein is described using in vitro data measured in C2C12 cells. Based on our results, we can state that septin proteins appear differently in the developmental stages of C2C12 cultures. We proved that cells cannot divide without Septin7 and that Septin7 is essential for the formation of myotubes. We have shown that the level of Septin7 contributes to the determination of cell shape and is an integral part of the cytoskeleton. Our measurements suggest that the level of Septin7 also affects the mitochondrial system of cells. We provide evidence that Septin7 filaments are rearranged during myoblast migration. Down-regulation of Septin7 expression resulted in altered migration parameters. Downregulation of Septin7 expression resulted in altered migration parameters. The specific role of Septin7 in the migration of myoblasts is also confirmed by FCF treatment. FCF inhibits C2C12 cell proliferation in a dose-dependent manner and presumably FCF treatment inhibits the dynamic rearrangement of septin filaments. Taken together, the Septin7 protein plays a fundamental role in the entirety of myoblast proliferation, differentiation, and migration processes, which are key events in the development and regeneration of functional skeletal muscle fibers.},
	keywords = {INTRACELLULAR CALCIUM; regeneration; skeletal muscle; Migració; CYTOSKELETON; myoblast; myogenesis; C2C12; vázizom; septin; migration; regeneráció; septin7; citoszkeleton; intracelluláris kalcium; miogenezis; Mioblaszt},
	year = {2024}
}

@article{MTMT:34484605,
	title = {Fluoxetine exerts anti‐inflammatory effects on human epidermal keratinocytes and suppresses their endothelin release},
	url = {https://m2.mtmt.hu/api/publication/34484605},
	author = {Tóth, Kinga Fanni and Ádám, Dorottya and Arany, József and Ramirez, Yesid A. and Bíró, Tamás and Drake, Jennifer I. and O'Mahony, Alison and Szöllősi, Attila and Póliska, Szilárd and Kilić, Ana and Soeberdt, Michael and Abels, Christoph and Oláh, Attila},
	doi = {10.1111/exd.14988},
	journal-iso = {EXP DERMATOL},
	journal = {EXPERIMENTAL DERMATOLOGY},
	volume = {33},
	unique-id = {34484605},
	issn = {0906-6705},
	abstract = {Fluoxetine is a safe antidepressant with remarkable anti‐inflammatory actions; therefore, we aimed to investigate its effects on immortalized (HaCaT) as well as primary human epidermal keratinocytes in a polyinosinic‐polycytidylic acid (p(I:C))‐induced inflammatory model. We found that a non‐cytotoxic concentration (MTT‐assay, CyQUANT‐assay) of fluoxetine significantly suppressed p(I:C)‐induced expression and release of several pro‐inflammatory cytokines (Q‐PCR, cytokine array, ELISA), and it decreased the release of the itch mediator endothelins (ELISA). These effects were not mediated by the inhibition of the NF‐κB or p38 MAPK pathways (western blot), or by the suppression of the p(I:C)‐induced elevation of mitochondrial ROS production (MitoSOX Red labeling). Instead, unbiased activity profiling revealed that they were most likely mediated via the inhibition of the phosphoinositide 3‐kinase (PI3K) pathway. Importantly, the PI3K‐inhibitor GDC0941 fully mimicked the effects of fluoxetine (Q‐PCR, ELISA). Although fluoxetine was able to occupy the binding site of GDC0941 (in silico molecular docking), and exerted direct inhibitory effect on PI3K (cell‐free PI3K activity assay), it exhibited much lower potency and efficacy as compared to GDC0941. Finally, RNA‐Seq analysis revealed that fluoxetine deeply influenced the transcriptional alterations induced by p(I:C)‐treatment, and exerted an overall anti‐inflammatory activity. Collectively, our findings demonstrate that fluoxetine exerts potent anti‐inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via interfering with the PI3K pathway. Thus, clinical studies are encouraged to explore whether the currently reported beneficial effects translate in vivo following its topical administration in inflammatory and pruritic dermatoses.},
	year = {2024},
	eissn = {1600-0625},
	orcid-numbers = {Ramirez, Yesid A./0000-0003-1399-8511; Drake, Jennifer I./0000-0002-2808-4475; O'Mahony, Alison/0000-0003-0510-6931; Kilić, Ana/0000-0001-5011-8734; Soeberdt, Michael/0000-0003-2594-9901; Abels, Christoph/0000-0002-7778-7740; Oláh, Attila/0000-0003-4122-5639}
}

@article{MTMT:34732773,
	title = {1026 NPR1 receptor expression in monocyte-derived langerhans cells},
	url = {https://m2.mtmt.hu/api/publication/34732773},
	author = {Horváth, Dorottya and Pénzes, Zsófia and Molnár, P. and Szöllősi, Attila},
	doi = {10.1016/j.jid.2023.03.1037},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	volume = {143},
	unique-id = {34732773},
	issn = {0022-202X},
	year = {2023},
	eissn = {1523-1747},
	pages = {S176-S176}
}

@article{MTMT:34729800,
	title = {Effect of anandamide on human monocyte-derived langerhans cell function},
	url = {https://m2.mtmt.hu/api/publication/34729800},
	author = {Pénzes, Zsófia and Horváth, Dorottya and Molnár, P. and Shahrzad, Alimohammadi and Szöllősi, Attila},
	doi = {10.1016/j.jid.2023.03.1038},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	volume = {143},
	unique-id = {34729800},
	issn = {0022-202X},
	year = {2023},
	eissn = {1523-1747},
	pages = {S176-S176}
}

@article{MTMT:34477780,
	title = {TRPM4-ioncsatornák vizsgálatának farmakológiai lehetőségei [=Pharmacological possibilities of testing TRPM4 ion channels]},
	url = {https://m2.mtmt.hu/api/publication/34477780},
	author = {Dienes, Csaba Bálint and Kovács, Zsigmond Máté and Óvári, József and Szentandrássy, Norbert},
	doi = {10.26430/CHUNGARICA.2023.53.5.446},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {34477780},
	issn = {0133-5596},
	abstract = {A tranziens receptorpotenciál melasztatin-4 a TRPM-fehérjecsalád egyedülálló tagja. A TRPM5-höz hasonlóan Ca2+-érzékeny és csak egyértékű kationokra permeábilis. Sok szervben, széles körben expresszálódik és a membránpotenciál és a Ca2+-homeosztázis szabályozásával számos funkcióval is bír mind az ingerlékeny, mind a nem ingerelhető sejtekben. Az áttekintés a TRPM4 farmakológiai modulációját tárgyalja az ioncsatorna egy régebbi, gyakrabban használt, valamint két újabb, potenciálisan szelektívebb inhibitorának összehasonlításával és leírásával. A TRPM4 egyre nagyobb figyelmet kap és valószínűleg a jövőben is a kutatások témája lesz.
		
		Summary
		The Transient Receptor Potential Melastatin 4 is a unique member of the TRPM protein family. Like TRPM5, it is Ca2+-sensitive and permeable only to monovalent cations. It is widely expressed in many organs and has multiple functions in both excitable and non-excitable cells by regulating membrane potential and Ca2+ homeostasis. This review discusses the pharmacological modulation of TRPM4 by comparing and describing one older, more commonly used inhibitor of the ion channel and two newer, potentially more selective inhibitors. TRPM4 is receiving increasing attention and is likely to be a topic of future research.},
	keywords = {9-phenanthrol; CBA; transient receptor potential melastatin 4 (TRPM4); meklofenamát; Meclofenamate},
	year = {2023},
	eissn = {1588-0230},
	pages = {446-450},
	orcid-numbers = {Szentandrássy, Norbert/0000-0003-0197-9567}
}

@article{MTMT:34193710,
	title = {The bZIP-type transcription factors NapA and RsmA modulate the volumetric ratio and the relative superoxide ratio of mitochondria in Aspergillus nidulans},
	url = {https://m2.mtmt.hu/api/publication/34193710},
	author = {Bákány, Bernadett and Antal, Réka and Szentesi, Péter and Emri, Tamás and Leiter, Éva Juliánna and Csernoch, László and Keller, Nancy P. and Pócsi, István and Dienes, Beatrix},
	doi = {10.1007/s42977-023-00184-1},
	journal-iso = {BIOL FUTURA},
	journal = {BIOLOGIA FUTURA},
	volume = {74},
	unique-id = {34193710},
	issn = {2676-8615},
	abstract = {Basic leucine zipper (bZIP) transcription factors are crucial components of differentiation, cellular homeostasis and the environmental stress defense of eukaryotes. In this work, we further studied the consequence of gene deletion and overexpression of two bZIP transcription factors, NapA and RsmA, on superoxide production, mitochondrial morphology and hyphal diameter of Aspergillus nidulans . We have found that reactive oxygen species production was influenced by both gene deletion and overexpression of napA under tert -butylhydroperoxide ( t BOOH) elicited oxidative stress. Furthermore, gene expression of napA negatively correlated with mitochondrial volumetric ratio as well as sterigmatocystin production of A. nidulans . High rsmA expression was accompanied with elevated relative superoxide ratio in the second hyphal compartment. A negative correlation between the expression of rsmA and catalase enzyme activity or mitochondrial volumetric ratio was also confirmed by statistical analysis. Hyphal diameter was independent on either rsmA and napA expression as well as 0.2 mM t BOOH treatment.},
	keywords = {bZIP-type transcription factors; Hyphal diameter; tBOOH stress; Superoxide level; Mitochondrial volumetric ratio},
	year = {2023},
	eissn = {2676-8607},
	pages = {337-346},
	orcid-numbers = {Szentesi, Péter/0000-0003-2621-2282}
}

@article{MTMT:34164432,
	title = {Nirmatrelvir, a novel medication for COVID-19 treatment},
	url = {https://m2.mtmt.hu/api/publication/34164432},
	author = {Hajian, Mohammad Reza and Jahantigh, Hamid Reza and Shahrzad, Alimohammadi and Mojtahedi, Zahra and Kianpour, Neda and Foroutan, Majid},
	doi = {10.34172/npj.2022.10486},
	journal-iso = {J NEPHROPHARMACOL},
	journal = {JOURNAL OF NEPHROPHARMACOLOGY},
	volume = {12},
	unique-id = {34164432},
	year = {2023},
	eissn = {2345-4202},
	orcid-numbers = {Hajian, Mohammad Reza/0000-0002-6854-0607; Jahantigh, Hamid Reza/0000-0002-0482-7510; Mojtahedi, Zahra/0000-0001-5133-7744; Kianpour, Neda/0000-0002-7096-648X; Foroutan, Majid/0000-0002-3691-2365}
}

@article{MTMT:34164428,
	title = {Crescentic glomerulonephritis in a man with a history of methamphetamine abuse; a possible cause for concern},
	url = {https://m2.mtmt.hu/api/publication/34164428},
	author = {Jahangiri, Dorsa and Ardalan, Mohammadreza and Mubarak, Muhammed and Shahrzad, Alimohammadi and Jahantigh, Hamid Reza and Saeifar, Sanam},
	doi = {10.34172/npj.2022.10508},
	journal-iso = {J NEPHROPHARMACOL},
	journal = {JOURNAL OF NEPHROPHARMACOLOGY},
	volume = {12},
	unique-id = {34164428},
	year = {2023},
	eissn = {2345-4202},
	orcid-numbers = {Jahangiri, Dorsa/0000-0003-1918-3583; Ardalan, Mohammadreza/0000-0002-6851-5460; Mubarak, Muhammed/0000-0001-6120-5884; Jahantigh, Hamid Reza/0000-0002-0482-7510; Saeifar, Sanam/0000-0001-5750-7070}
}