@article{MTMT:34804106,
	title = {MicroRNA-Mediated Suppression of Glial Cell Line-Derived Neurotrophic Factor Expression Is Modulated by a Schizophrenia-Associated Non-Coding Polymorphism},
	url = {https://m2.mtmt.hu/api/publication/34804106},
	author = {Keszler, Gergely and Vékony, Bálint and Elek, Zsuzsanna and Nemoda, Zsófia and Angyal, Nóra and Bánlaki, Zsófia and Kovács-Nagy, Réka and Rónai, Zsolt and Réthelyi, János},
	doi = {10.3390/ijms25084477},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34804106},
	issn = {1661-6596},
	abstract = {Plasma levels of glial cell line-derived neurotrophic factor (GDNF), a pivotal regulator of differentiation and survival of dopaminergic neurons, are reportedly decreased in schizophrenia. To explore the involvement of GDNF in the pathogenesis of the disease, a case–control association analysis was performed between five non-coding single nucleotide polymorphisms (SNP) across the GDNF gene and schizophrenia. Of them, the ‘G’ allele of the rs11111 SNP located in the 3′ untranslated region (3′-UTR) of the gene was found to associate with schizophrenia. In silico analysis revealed that the rs11111 ‘G’ allele might create binding sites for three microRNA (miRNA) species. To explore the significance of this polymorphism, transient co-transfection assays were performed in human embryonic kidney 293T (HEK293T) cells with a luciferase reporter construct harboring either the ‘A’ or ‘G’ allele of the 3′-UTR of GDNF in combination with the hsa-miR-1185-1-3p pre-miRNA. It was demonstrated that in the presence of the rs11111 ‘G’ (but not the ‘A’) allele, hsa-miR-1185-2-3p repressed luciferase activity in a dose-dependent manner. Deletion of the miRNA binding site or its substitution with the complementary sequence abrogated the modulatory effect. Our results imply that the rs11111 ‘G’ allele occurring more frequently in patients with schizophrenia might downregulate GDNF expression in a miRNA-dependent fashion.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Vékony, Bálint/0000-0002-6814-7311; Nemoda, Zsófia/0000-0002-9550-7730; Bánlaki, Zsófia/0000-0002-3815-422X; Rónai, Zsolt/0000-0002-0909-7932; Réthelyi, János/0000-0002-3641-012X}
}

@article{MTMT:34154205,
	title = {Persistent sepsis-induced transcriptomic signatures in signaling pathways of peripheral blood leukocytes: A pilot study},
	url = {https://m2.mtmt.hu/api/publication/34154205},
	author = {Elek, Zsuzsanna and Losoncz, Eszter and Fülep, Z. and Kovács-Nagy, Réka and Bánlaki, Zsófia and Szlobodnyik, G. and Keszler, Gergely and Rónai, Zsolt},
	doi = {10.1016/j.humimm.2023.08.146},
	journal-iso = {HUM IMMUNOL},
	journal = {HUMAN IMMUNOLOGY},
	volume = {84},
	unique-id = {34154205},
	issn = {0198-8859},
	year = {2023},
	eissn = {1879-1166},
	pages = {600-608},
	orcid-numbers = {Losoncz, Eszter/0000-0001-6426-8821; Bánlaki, Zsófia/0000-0002-3815-422X; Rónai, Zsolt/0000-0002-0909-7932}
}

@article{MTMT:33734164,
	title = {Missense Variants of von Willebrand Factor in the Background of COVID-19 Associated Coagulopathy},
	url = {https://m2.mtmt.hu/api/publication/33734164},
	author = {Molnár, Zsuzsanna and Losoncz, Eszter and Maricza, Katalin and Fülep, Z. and Bánlaki, Zsófia and Kovács-Nagy, Réka and Keszler, Gergely and Rónai, Zsolt},
	doi = {10.3390/genes14030617},
	journal-iso = {GENES-BASEL},
	journal = {GENES},
	volume = {14},
	unique-id = {33734164},
	issn = {2073-4425},
	abstract = {COVID-19 associated coagulopathy (CAC), characterized by endothelial dysfunction and hypercoagulability, evokes pulmonary immunothrombosis in advanced COVID-19 cases. Elevated von Willebrand factor (vWF) levels and reduced activities of the ADAMTS13 protease are common in CAC. Here, we aimed to determine whether common genetic variants of these proteins might be associated with COVID-19 severity and hemostatic parameters. A set of single nucleotide polymorphisms (SNPs) in the vWF (rs216311, rs216321, rs1063856, rs1800378, rs1800383) and ADAMTS13 genes (rs2301612, rs28729234, rs34024143) were genotyped in 72 COVID-19 patients. Cross-sectional cohort analysis revealed no association of any polymorphism with disease severity. On the other hand, analysis of variance (ANOVA) uncovered associations with the following clinical parameters: (1) the rs216311 T allele with enhanced INR (international normalized ratio); (2) the rs1800383 C allele with elevated fibrinogen levels; and (3) the rs1063856 C allele with increased red blood cell count, hemoglobin, and creatinine levels. No association could be observed between the phenotypic data and the polymorphisms in the ADAMTS13 gene. Importantly, in silico protein conformational analysis predicted that these missense variants would display global conformational alterations, which might affect the stability and plasma levels of vWF. Our results imply that missense vWF variants might modulate the thrombotic risk in COVID-19.},
	keywords = {Protein Conformation; Single nucleotide polymorphism (SNP); von Willebrand factor; ADAMTS13; immunothrombosis; missense variant; COVID-19 associated coagulopathy},
	year = {2023},
	eissn = {2073-4425},
	orcid-numbers = {Molnár, Zsuzsanna/0000-0002-4598-3608; Losoncz, Eszter/0000-0001-6426-8821; Maricza, Katalin/0009-0007-9361-2135; Bánlaki, Zsófia/0000-0002-3815-422X; Rónai, Zsolt/0000-0002-0909-7932}
}

@article{MTMT:32761919,
	title = {Complement Factor H-Related Proteins FHR1 and FHR5 Interact With Extracellular Matrix Ligands, Reduce Factor H Regulatory Activity and Enhance Complement Activation},
	url = {https://m2.mtmt.hu/api/publication/32761919},
	author = {Papp, Alexandra Éva and Papp, Krisztián and Uzonyi, Barbara and Cserhalmi, Marcell and Csincsi, Ádám and Szabó, Zsóka and Bánlaki, Zsófia and Ermert, David and Prohászka, Zoltán and Erdei, Anna and Ferreira, Viviana P. and Blom, Anna M. and Józsi, Mihály},
	doi = {10.3389/fimmu.2022.845953},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {13},
	unique-id = {32761919},
	issn = {1664-3224},
	year = {2022},
	eissn = {1664-3224},
	orcid-numbers = {Papp, Krisztián/0000-0003-0619-8233; Uzonyi, Barbara/0000-0002-9680-1974; Bánlaki, Zsófia/0000-0002-3815-422X; Prohászka, Zoltán/0000-0003-1761-7982; Erdei, Anna/0000-0002-3622-6680; Józsi, Mihály/0000-0002-5520-5535}
}

@article{MTMT:31607929,
	title = {Correlation between Expression Profiles of Key Signaling Genes in Colorectal Cancer Samples from Type 2 Diabetic and Non-Diabetic Patients},
	url = {https://m2.mtmt.hu/api/publication/31607929},
	author = {Molnár, Zsuzsanna and Rónai, Zsolt and Keszler, Gergely and Harsányi, László and Kontsek, Endre and Herold, Zoltán and Herold, Magdolna and Somogyi, Anikó and Bánlaki, Zsófia},
	doi = {10.3390/life10090216},
	journal-iso = {LIFE-BASEL},
	journal = {LIFE-BASEL},
	volume = {10},
	unique-id = {31607929},
	abstract = {Several lines of epidemiological and biochemical evidence support the association of type 2 diabetes mellitus (T2DM) and colorectal cancer (CRC). T2DM has been shown to impinge on the transcriptome of colon tumor cells, promoting their proliferation and invasion. In order to gain insight into diabetes-specific modulation of colon cancer signaling, we analyzed gene expression patterns of more than five hundred genes encoding signaling proteins on TaqMan OpenArray panels from colonoscopic colorectal tumor samples of type 2 diabetic and non-diabetic patients. In total, 48 transcripts were found to be differentially expressed in tumors of T2DM patients as compared to healthy colon samples. Enrichment analysis with the g:GOSt (Gene Ontology Statistics) functional profiling tool revealed that the underlying genes can be classified into five signaling pathways (in decreasing order of significance: Wnt (wingless-type)/beta-catenin; Hippo; TNF (tumor necrosis factor); PI3K/Akt (phosphoinositide-3 kinase/protein kinase B), and platelet activation), implying that targeted downregulation of these signaling cascades might help combat CRC in diabetic patients. Transcript levels of some of the differentially expressed genes were also measured from surgically removed diabetic and non-diabetic CRC specimens by individual qPCR (quantitative real-time PCR) assays using the adjacent normal tissue mRNA levels as an internal control. The most significantly altered genes in diabetic tumor samples were largely different from those in non-diabetic ones, implying that T2DM profoundly alters the expression of signaling genes and presumably the biological characteristics of CRC.},
	year = {2020},
	eissn = {2075-1729},
	orcid-numbers = {Molnár, Zsuzsanna/0000-0002-4598-3608; Rónai, Zsolt/0000-0002-0909-7932; Harsányi, László/0000-0003-2657-0039; Kontsek, Endre/0000-0002-8098-1392; Herold, Zoltán/0000-0001-5990-4889; Herold, Magdolna/0000-0002-1036-6343; Somogyi, Anikó/0000-0003-0807-260X; Bánlaki, Zsófia/0000-0002-3815-422X}
}

@article{MTMT:31305664,
	title = {Diabetes-specific modulation of peripheral blood gene expression signatures in colorectal cancer},
	url = {https://m2.mtmt.hu/api/publication/31305664},
	author = {Molnár, Zsuzsanna and Bánlaki, Zsófia and Somogyi, Anikó and Herold, Zoltán and Herold, Magdolna and Guttman, András and Rónai, Zsolt and Keszler, Gergely},
	doi = {10.2174/1566524020666200504084626},
	journal-iso = {CURR MOL MED},
	journal = {CURRENT MOLECULAR MEDICINE},
	volume = {20},
	unique-id = {31305664},
	issn = {1566-5240},
	year = {2020},
	eissn = {1875-5666},
	pages = {773-780},
	orcid-numbers = {Molnár, Zsuzsanna/0000-0002-4598-3608; Bánlaki, Zsófia/0000-0002-3815-422X; Somogyi, Anikó/0000-0003-0807-260X; Herold, Zoltán/0000-0001-5990-4889; Herold, Magdolna/0000-0002-1036-6343; Guttman, András/0000-0002-7838-082X; Rónai, Zsolt/0000-0002-0909-7932; Keszler, Gergely/0000-0002-0528-0238}
}

@article{MTMT:30686443,
	title = {DNA Methylation, Speciation and Domestication},
	url = {https://m2.mtmt.hu/api/publication/30686443},
	author = {Bánlaki, Zsófia},
	doi = {10.4172/2379-1764.1000234},
	journal-iso = {ADV TECHN BIOL MED},
	journal = {ADVANCED TECHNIQUES IN BIOLOGY & MEDICINE},
	volume = {5},
	unique-id = {30686443},
	issn = {2379-1764},
	year = {2017},
	orcid-numbers = {Bánlaki, Zsófia/0000-0002-3815-422X}
}

@article{MTMT:3238361,
	title = {DNA methylation patterns of behavior-related gene promoter regions dissect the gray wolf from domestic dog breeds},
	url = {https://m2.mtmt.hu/api/publication/3238361},
	author = {Bánlaki, Zsófia and Cimarelli, G and Viranyi, Z and Kubinyi, Enikő and Sasvári-Székely, Mária and Rónai, Zsolt},
	doi = {10.1007/s00438-017-1305-5},
	journal-iso = {MOL GENET GENOMICS},
	journal = {MOLECULAR GENETICS AND GENOMICS},
	volume = {292},
	unique-id = {3238361},
	issn = {1617-4615},
	abstract = {A growing body of evidence highlights the relationship between epigenetics, especially DNA methylation, and population divergence as well as speciation. However, little is known about how general the phenomenon of epigenetics-wise separation of different populations is, or whether population assignment is, possible based on solely epigenetic marks. In the present study, we compared DNA methylation profiles between four different canine populations: three domestic dog breeds and their ancestor the gray wolf. Altogether, 79 CpG sites constituting the 65 so-called CpG units located in the promoter regions of genes affecting behavioral and temperamental traits (COMT, HTR1A, MAOA, OXTR, SLC6A4, TPH1, WFS1)-regions putatively targeted during domestication and breed selection. Methylation status of buccal cells was assessed using EpiTYPER technology. Significant inter-population methylation differences were found in 52.3% of all CpG units investigated. DNA methylation profile-based hierarchical cluster analysis indicated an unambiguous segregation of wolf from domestic dog. In addition, one of the three dog breeds (Golden Retriever) investigated also formed a separate, autonomous group. The findings support that population segregation is interrelated with shifts in DNA methylation patterns, at least in putative selection target regions, and also imply that epigenetic profiles could provide a sufficient basis for population assignment of individuals.},
	keywords = {BEHAVIOR; MONOAMINE-OXIDASE; PROMOTER; HUMAN BRAIN; DNA methylation; Canine; ARTIFICIAL SELECTION; MEMORY FORMATION; Domestication; NEUROTROPHIC FACTOR BDNF; OPEN-ACCESS DATABASE; oxytocin receptor gene; epigenetic inheritance; SOUTHERN EAST-ASIA; FACTOR-BINDING PROFILES; Population assignment},
	year = {2017},
	eissn = {1617-4623},
	pages = {685-697},
	orcid-numbers = {Bánlaki, Zsófia/0000-0002-3815-422X; Kubinyi, Enikő/0000-0002-4468-9845; Sasvári-Székely, Mária/0000-0002-7029-4337; Rónai, Zsolt/0000-0002-0909-7932}
}

@article{MTMT:3227977,
	title = {Social Behavior of Pet Dogs Is Associated with Peripheral OXTR Methylation},
	url = {https://m2.mtmt.hu/api/publication/3227977},
	author = {Cimarelli, G and Viranyi, Z and Turcsán, Borbála and Rónai, Zsolt and Sasvári-Székely, Mária and Bánlaki, Zsófia},
	doi = {10.3389/fpsyg.2017.00549},
	journal-iso = {FRONT PSYCHOL},
	journal = {FRONTIERS IN PSYCHOLOGY},
	volume = {8},
	unique-id = {3227977},
	issn = {1664-1078},
	abstract = {Oxytocin is a key modulator of emotional processing and social cognitive function. In line with this, polymorphisms of genes involved in oxytocin signaling, like the oxytocin receptor (OXTR) gene, are known to influence social behavior in various species. However, to date, no study has investigated environmental factors possibly influencing the epigenetic variation of the OXTR gene and its behavioral effects in dogs. Pet dogs form individualized and strong relationships with their owners who are central figures in the social environment of their dogs and therefore might influence the methylation levels of their OXTR gene. Here we set out to investigate whether DNA methylation within the OXTR promoter region of pet dogs is linked to their owner's interaction style and to the social behavior of the dogs. To be able to do so, we collected buccal epithelial cells and, in Study 1, we used pyrosequencing techniques to look for differentially methylated CpG sites in the canine OXTR promoter region on a heterogeneous sample of dogs and wolves of different ages and keeping conditions. Four identified sites (at positions -727, -751, -1371, and -1383 from transcription start site) showing more than 10% methylation variation were then, in Study 2, measured in triplicate in 217 pet Border Collies previously tested for reactions to an adverse social situation (i.e., approach by a threatening human) and with available data on their owners' interaction styles. We found that CpG methylation was significantly associated with the behavior of the dogs, in particular with the likelihood that dogs would hide behind their owner or remain passive when approached by a threatening human. On the other hand, CpG methylation was not related to the owners' behavior but to dog sex (at position -1371). Our findings underpin the complex relationship between epigenetics and behavior and highlight the importance of including epigenetic methods in the analysis of dog behavioral development. Further research is needed to investigate which environmental factors influence the epigenetic variation of the OXTR gene.},
	year = {2017},
	eissn = {1664-1078},
	orcid-numbers = {Turcsán, Borbála/0000-0002-0197-5243; Rónai, Zsolt/0000-0002-0909-7932; Sasvári-Székely, Mária/0000-0002-7029-4337; Bánlaki, Zsófia/0000-0002-3815-422X}
}

@article{MTMT:3221358,
	title = {FHR-1 binds to C-reactive protein and enhances rather than inhibits complement activation},
	url = {https://m2.mtmt.hu/api/publication/3221358},
	author = {Csincsi, Ádám and Weiszhar, Zsóka and Bánlaki, Zsófia and Uzonyi, Barbara and Cserhalmi, Marcell and Kárpáti, Éva and Tortajada, A and Caesar, JJE and Prohászka, Zoltán and Jokiranta, TS and Lea, SM and Rodríguez, de Córdoba S and Józsi, Mihály},
	doi = {10.4049/jimmunol.1600483},
	journal-iso = {J IMMUNOL},
	journal = {JOURNAL OF IMMUNOLOGY},
	volume = {199},
	unique-id = {3221358},
	issn = {0022-1767},
	abstract = {Factor H-related protein (FHR) 1 is one of the five human FHRs that share sequence and structural homology with the alternative pathway complement inhibitor FH. Genetic studies on disease associations and functional analyses indicate that FHR-1 enhances complement activation by competitive inhibition of FH binding to some surfaces and immune proteins. We have recently shown that FHR-1 binds to pentraxin 3. In this study, our aim was to investigate whether FHR-1 binds to another pentraxin, C-reactive protein (CRP), analyze the functional relevance of this interaction, and study the role of FHR-1 in complement activation and regulation. FHR-1 did not bind to native, pentameric CRP, but it bound strongly to monomeric CRP via its C-terminal domains. FHR-1 at high concentration competed with FH for CRP binding, indicating possible complement deregulation also on this ligand. FHR-1 did not inhibit regulation of solid-phase C3 convertase by FH and did not inhibit terminal complement complex formation induced by zymosan. On the contrary, by binding C3b, FHR-1 allowed C3 convertase formation and thereby enhanced complement activation. FHR-1/CRP interactions increased complement activation via the classical and alternative pathways on surfaces such as the extracellular matrix and necrotic cells. Altogether, these results identify CRP as a ligand for FHR-1 and suggest that FHR-1 enhances, rather than inhibits, complement activation, which may explain the protective effect of FHR-1 deficiency in age-related macular degeneration.},
	year = {2017},
	eissn = {1550-6606},
	pages = {292-303},
	orcid-numbers = {Bánlaki, Zsófia/0000-0002-3815-422X; Uzonyi, Barbara/0000-0002-9680-1974; Prohászka, Zoltán/0000-0003-1761-7982; Józsi, Mihály/0000-0002-5520-5535}
}