@article{MTMT:3333944, title = {Coordinated activation of a cluster of MMP genes in response to UVB radiation}, url = {https://m2.mtmt.hu/api/publication/3333944}, author = {Újfaludi, Zsuzsanna and Tuzesi, Agota and Majoros, Hajnalka and Rothler, Bálint and Pankotai, Tibor and Boros, Imre Miklós}, doi = {10.1038/s41598-018-20999-6}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {8}, unique-id = {3333944}, year = {2018}, eissn = {2045-2322}, orcid-numbers = {Újfaludi, Zsuzsanna/0000-0003-4738-0963; Majoros, Hajnalka/0000-0003-2020-971X; Pankotai, Tibor/0000-0001-9810-5465; Boros, Imre Miklós/0000-0001-8504-9687} } @article{MTMT:3170378, title = {Human p53 interacts with the elongating RNAPII complex and is required for the release of actinomycin D induced transcription blockage}, url = {https://m2.mtmt.hu/api/publication/3170378}, author = {Borsos, Barbara Nikolett and Huliák, Ildikó and Majoros, Hajnalka and Újfaludi, Zsuzsanna and Gyenis, A and Pukler, P and Boros, Imre Miklós and Pankotai, Tibor}, doi = {10.1038/srep40960}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {7}, unique-id = {3170378}, abstract = {The p53 tumour suppressor regulates the transcription initiation of selected genes by binding to specific DNA sequences at their promoters. Here we report a novel role of p53 in transcription elongation in human cells. Our data demonstrate that upon transcription elongation blockage, p53 is associated with genes that have not been reported as its direct targets. p53 could be co-immunoprecipitated with active forms of DNA-directed RNA polymerase II subunit 1 (RPB1), highlighting its association with the elongating RNA polymerase II. During a normal transcription cycle, p53 and RPB1 are localised at distinct regions of selected non-canonical p53 target genes and this pattern of localisation was changed upon blockage of transcription elongation. Additionally, transcription elongation blockage induced the proteasomal degradation of RPB1. Our results reveal a novel role of p53 in human cells during transcription elongation blockage that may facilitate the removal of RNA polymerase II from DNA.}, year = {2017}, eissn = {2045-2322}, orcid-numbers = {Majoros, Hajnalka/0000-0003-2020-971X; Újfaludi, Zsuzsanna/0000-0003-4738-0963; Boros, Imre Miklós/0000-0001-8504-9687; Pankotai, Tibor/0000-0001-9810-5465} } @article{MTMT:3237714, title = {Splicing factors differentially expressed in psoriasis alter mRNA maturation of disease-associated EDA+ fibronectin.}, url = {https://m2.mtmt.hu/api/publication/3237714}, author = {Szlávicz, Eszter and Szabó, Kornélia Ágnes and Groma, Gergely and Csörgő Sándorné Bata, Zsuzsanna and Pagani, F and Kemény, Lajos and Széll, Márta}, doi = {10.1007/s11010-017-3090-1}, journal-iso = {MOL CELL BIOCHEM}, journal = {MOLECULAR AND CELLULAR BIOCHEMISTRY}, volume = {436}, unique-id = {3237714}, issn = {0300-8177}, abstract = {The EDA+ fibronectin splicing variant is overexpressed in psoriatic non-lesional epidermis and sensitizes keratinocytes to mitogenic signals. However, regulation of its abundance is only partially understood. In our recent cDNA microarray experiment, we identified three SR-rich splicing factors-splicing factor, arginine/serine-rich 18 (SFRS18), peptidyl-prolyl cis-trans isomerase G (PPIG), and luc-7 like protein 3 (LUC7L3)-which might be implicated in the preactivated states of keratinocytes in psoriatic non-involved skin and could also contribute to the regulation of fibronectin mRNA maturation. In this study, we investigated the role of LUC7L3, PPIG, and SFRS18 in psoriasis and in the mRNA maturation process of fibronectin. Regarding tissue staining experiments, we were able to demonstrate a characteristic distribution of the splicing factors in healthy, psoriatic non-involved and involved epidermis. Moreover, the expression profiles of these SR-rich proteins were found to be very similar in synchronized keratinocytes. Contribution of splicing facwwtors to the EDA+ fibronectin formation was also confirmed: their siRNA silencing leads to altered fibronectin mRNA and protein expression patterns, suggesting the participation in the EDA domain inclusion. Our results indicate that LUC7L3, PPIG, and SFRS18 are not only implicated in EDA+ fibronectin formation, but also that they could possess multiple roles in psoriasis-associated molecular abnormalities.}, year = {2017}, eissn = {1573-4919}, pages = {189-199}, orcid-numbers = {Szlávicz, Eszter/0000-0002-1083-0994; Szabó, Kornélia Ágnes/0000-0002-6231-3251; Groma, Gergely/0000-0001-8487-0465; Csörgő Sándorné Bata, Zsuzsanna/0000-0002-3732-1743; Kemény, Lajos/0000-0002-2119-9501; Széll, Márta/0000-0002-0730-714X} }