TY - JOUR AU - Chi, Yanting AU - Qin, Zhiming AU - Qiu, Jingjing AU - Li, Binbin TI - Integrated study of DNA methylation and transcriptome: a new perspective for exploring the pathogenesis of Sjögren's syndrome JF - EPIGENETICS & CHROMATIN J2 - EPIGENET CHROMATIN VL - 18 PY - 2025 IS - 1 PG - 16 SN - 1756-8935 DO - 10.1186/s13072-025-00637-y UR - https://m2.mtmt.hu/api/publication/36444536 ID - 36444536 N1 - Funding Agency and Grant Number: CAMS Innovation Fund for Medical Sciences [2019-I2M-5-038] Funding text: This study was supported by the CAMS Innovation Fund for Medical Sciences (2019-I2M-5-038). AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Czárán, Domonkos Tamás AU - Sasvári, Péter AU - Lőrincz, Kende Kálmán AU - Ella, Krisztina AU - Gellén, Virág AU - Csépányi-Kömi, Roland TI - ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 16 PY - 2025 PG - 17 SN - 1664-3224 DO - 10.3389/fimmu.2025.1509713 UR - https://m2.mtmt.hu/api/publication/35792375 ID - 35792375 N1 - Funding Agency and Grant Number: National Research Development and Innovation Office, Hungary [FK_18 128376, TKP2021-EGA-24, TKP2021-EGA-25]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences [EFOP-3.6.3-VEKOP-16-2017-00009] Funding text: The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This research was funded by research grant No. FK_18 128376 to R. Cs-K., TKP2021-EGA-24 and TKP2021-EGA-25 from the National Research Development and Innovation Office, Hungary. The project also received funding from the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences to R. Cs-K. and K. E. The SE250+ Excellence PhD Scholarship supported D. Cz. and P. S. (EFOP-3.6.3-VEKOP-16-2017-00009). LA - English DB - MTMT ER - TY - JOUR AU - Wu, Yan AU - Jiang, Wen AU - Wang, Jianhong TI - Integrating Genomic, eQTL, and Mendelian Randomization Analyses to Identify Microglial Drug Targets in Multiple Sclerosis JF - JOURNAL OF CELLULAR AND MOLECULAR MEDICINE J2 - J CELL MOL MED VL - 29 PY - 2025 IS - 22 PG - 11 SN - 1582-1838 DO - 10.1111/jcmm.70754 UR - https://m2.mtmt.hu/api/publication/36762386 ID - 36762386 LA - English DB - MTMT ER - TY - JOUR AU - Hong, Q. AU - Hu, H. AU - Liu, D. AU - Hu, X. AU - Wang, Z. AU - Zhou, D. TI - Bioinformatic analysis of differentially expressed genes in lung cancer bone metastasis and their implications for disease progression in lung cancer patients JF - JOURNAL OF THORACIC DISEASE J2 - J THORACIC DISEASE VL - 16 PY - 2024 IS - 7 SP - 4666 EP - 4677 PG - 12 SN - 2072-1439 DO - 10.21037/jtd-24-1081 UR - https://m2.mtmt.hu/api/publication/35187565 ID - 35187565 N1 - Export Date: 28 August 2024 LA - English DB - MTMT ER - TY - JOUR AU - Sasvári, Péter AU - Pettkó-Szandtner, Aladár AU - Wisniewski, Éva AU - Csépányi-Kömi, Roland TI - Neutrophil-specific interactome of ARHGAP25 reveals novel partners and regulatory insights JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 14 PY - 2024 IS - 1 PG - 13 SN - 2045-2322 DO - 10.1038/s41598-024-71002-4 UR - https://m2.mtmt.hu/api/publication/35217359 ID - 35217359 AB - 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. LA - English DB - MTMT ER -