@article{MTMT:36444536,
	title = {Integrated study of DNA methylation and transcriptome: a new perspective for exploring the pathogenesis of Sjögren's syndrome},
	url = {https://m2.mtmt.hu/api/publication/36444536},
	author = {Chi, Yanting and Qin, Zhiming and Qiu, Jingjing and Li, Binbin},
	doi = {10.1186/s13072-025-00637-y},
	journal-iso = {EPIGENET CHROMATIN},
	journal = {EPIGENETICS & CHROMATIN},
	volume = {18},
	unique-id = {36444536},
	issn = {1756-8935},
	abstract = {Background/PurposeSj & ouml;gren's syndrome (SS) is a chronic systemic autoimmune disease characterized by lymphocytic infiltration and formation of lymphoepithelial lesions (LEL) in exocrine glands, leading to secretory dysfunction. DNA methylation, a dynamically regulated epigenetic mark, has been increasingly recognized as a key regulatory mechanism in the pathogenesis of autoimmune diseases including SS, and holds promise for identifying novel diagnostic and therapeutic strategies.MethodsReduced representation bisulfite sequencing (RRBS) was performed on 4 cases of SS and 3 controls to profile genome-wide DNA methylation patterns. Differentially methylated regions (DMRs) and associated differentially methylated genes (DMGs) were detected, followed by functional enrichment analysis. Integration with transcriptomic data (GSE40611) was performed to identify overlapping epigenetic and transcriptional changes.ResultsA total of 29,462 DMRs were detected, with 24,116 hypermethylated and 5,346 hypomethylated regions, indicating an overall increase in methylation levels of SS, and DMGs located in gene promoter regions were significantly enriched in pathways related to immune response, transcriptional regulation, and inflammation. Nine hub genes (LCP2, BTK, LAPTM5, ARHGAP9, IKZF1, WDFY4, CSF2RB, ARHGAP25, DOCK8) were identified, which displayed promoter hyper-or hypomethylation, indicating the complex epigenetic regulatory mechanisms.ConclusionThis study reveals extensive DNA methylation alterations in SS, providing new insights into the epigenetic mechanisms underlying pathogenesis. Moreover, these findings suggest potential biomarkers or therapeutic targets for further investigation to elucidate detailed molecular mechanisms of SS.},
	keywords = {Inflammation; DNA methylation; SJOGRENS-SYNDROME; Transcriptome; CYTOSCAPE; Reduced representation bisulfite sequencing; Gren's syndrome; Sj & ouml},
	year = {2025},
	eissn = {1756-8935}
}

@article{MTMT:35792375,
	title = {ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity},
	url = {https://m2.mtmt.hu/api/publication/35792375},
	author = {Czárán, Domonkos Tamás and Sasvári, Péter and Lőrincz, Kende Kálmán and Ella, Krisztina and Gellén, Virág and Csépányi-Kömi, Roland},
	doi = {10.3389/fimmu.2025.1509713},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {16},
	unique-id = {35792375},
	issn = {1664-3224},
	year = {2025},
	eissn = {1664-3224},
	orcid-numbers = {Czárán, Domonkos Tamás/0000-0003-3438-1094; Lőrincz, Kende Kálmán/0000-0002-1861-1008; Ella, Krisztina/0000-0003-4961-5615; Csépányi-Kömi, Roland/0000-0001-6825-7142}
}

@article{MTMT:36762386,
	title = {Integrating Genomic, eQTL, and Mendelian Randomization Analyses to Identify Microglial Drug Targets in Multiple Sclerosis},
	url = {https://m2.mtmt.hu/api/publication/36762386},
	author = {Wu, Yan and Jiang, Wen and Wang, Jianhong},
	doi = {10.1111/jcmm.70754},
	journal-iso = {J CELL MOL MED},
	journal = {JOURNAL OF CELLULAR AND MOLECULAR MEDICINE},
	volume = {29},
	unique-id = {36762386},
	issn = {1582-1838},
	keywords = {Multiple sclerosis (MS); microglia; single-cell sequencing; Mendelian randomization (MR); Bayesian colocalization; cis-eQTL analysis},
	year = {2025},
	eissn = {1582-4934}
}

@article{MTMT:35187565,
	title = {Bioinformatic analysis of differentially expressed genes in lung cancer bone metastasis and their implications for disease progression in lung cancer patients},
	url = {https://m2.mtmt.hu/api/publication/35187565},
	author = {Hong, Q. and Hu, H. and Liu, D. and Hu, X. and Wang, Z. and Zhou, D.},
	doi = {10.21037/jtd-24-1081},
	journal-iso = {J THORACIC DISEASE},
	journal = {JOURNAL OF THORACIC DISEASE},
	volume = {16},
	unique-id = {35187565},
	issn = {2072-1439},
	year = {2024},
	eissn = {2077-6624},
	pages = {4666-4677}
}

@article{MTMT:35217359,
	title = {Neutrophil-specific interactome of ARHGAP25 reveals novel partners and regulatory insights},
	url = {https://m2.mtmt.hu/api/publication/35217359},
	author = {Sasvári, Péter and Pettkó-Szandtner, Aladár and Wisniewski, Éva and Csépányi-Kömi, Roland},
	doi = {10.1038/s41598-024-71002-4},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {14},
	unique-id = {35217359},
	abstract = {ARHGAP25, a crucial molecule in immunological processes, serves as a Rac-specific GTPase-activating protein. Its role in cell migration and phagocyte functions, affecting the outcome of complex immunological diseases such as rheumatoid arthritis, renders it a promising target for drug research. Despite its importance, our knowledge of its intracellular interactions is still limited. This study employed proteomic analysis of glutathione S-transferase (GST)-tag pulldowns and co-immunoprecipitation from neutrophilic granulocyte cell lysate, revealing 76 candidates for potential physical interactions that complement ARHGAP25’s known profile. Notably, four small GTPases (RAC2, RHOG, ARF4, and RAB27A) exhibited high affinity for ARHGAP25. The ARHGAP25–RAC2 and ARHGAP25–RHOG interactions appeared to be affected by the activation state of the small GTPases, suggesting a GTP–GDP cycle-dependent interaction. In silico dimer prediction pinpointed ARHGAP25’s GAP domain as a credible binding interface, suggesting its suitability for GTP hydrolysis. Additionally, a list of Fc receptor-related kinases, phosphatases, and three of the 14-3-3 members were identified as potential partners, with in silico predictions highlighting eight binding sites, presenting novel insight on a potential regulatory mechanism for ARHGAP25.},
	year = {2024},
	eissn = {2045-2322},
	orcid-numbers = {Wisniewski, Éva/0000-0001-8698-6867; Csépányi-Kömi, Roland/0000-0001-6825-7142}
}