@mastersthesis{MTMT:33095648,
	title = {A PARI fehérje szerepe a rekombináció-függő folyamatok szabályozásában elakadt replikációs villa esetén [The role of the PARI protein in the regulation of recombination-dependent mechanisms at the stalled replication fork]},
	url = {https://m2.mtmt.hu/api/publication/33095648},
	author = {Hegedűs, Lili},
	doi = {10.14232/phd.11049},
	publisher = {SZTE},
	unique-id = {33095648},
	abstract = {Egy DNS-hiba következtében elakadt replikációs villa menekítése többféleképpen is megvalósulhat a sejtekben. Az, hogy melyik útvonal aktív, szigorú szabályozás alatt áll, hiszen nem mindegy, hogy a sejtekben egy gyors, ám mutagén transzléziós szintézis zajlik vagy éppen egy bonyolult struktúrákon végbemenő, de pontos másolást lehetővé tevő templátváltás. Ezen mechanizmusok közötti molekuláris kapcsoló a PCNA fehérje, illetve annak poszttranszlációs módosításai. Míg ubiquitilációja a DNS-hibatolerancia útvonalakat aktiválja, addig SUMOilációja a rekombináció-függő folyamatot gátolja. Utóbbiban élesztőben végzett vizsgálatok alapján fontos szerepet tölt be az Srs2 fehérje, több szinten hatva. Helikáz aktivitása révén részt vesz a D-hurok szétszerelésében, SUMOilált PCNA-függő módon pedig a D-hurok meghosszabbítását gátolja. Humán sejtekben ezeket a funkciókat több fehérje látja el, melyek közül a PARI-ról mutatták ki, hogy kölcsönhatásba lép a SUMOilált PCNA-vel. Munkánk során azt vizsgáltuk, hogy a PARI fehérje milyen molekuláris mechanizmusok révén valósítja meg a homológ rekombináció gátlását az elakadt replikációs villa menekítésekor: a D-hurok meghosszabbításának gátlása során megakadályozza, hogy a homológ szakaszról hosszasan történjen meg a duplikáció, lecsökkentve az esélyét az átkereszteződéseknek és meggátolva a további rekombinációs eseményeket és az esetleges genomi átrendeződéseket.},
	year = {2022}
}

@article{MTMT:30791081,
	title = {Multilevel structure–activity profiling reveals multiple green tea compound families that each modulate ubiquitin-activating enzyme and ubiquitination by a distinct mechanism},
	url = {https://m2.mtmt.hu/api/publication/30791081},
	author = {Fenteany, Gabriel and Gaur, Paras and Hegedűs, Lili and Dudás, Kata and Kiss, Ernő and Wéber, Edit and Hackler, László and Martinek, Tamás and Puskás, László and Haracska, Lajos},
	doi = {10.1038/s41598-019-48888-6},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {9},
	unique-id = {30791081},
	issn = {2045-2322},
	year = {2019},
	eissn = {2045-2322},
	orcid-numbers = {Fenteany, Gabriel/0000-0001-7407-2195; Kiss, Ernő/0000-0002-7344-1750; Wéber, Edit/0000-0002-5904-0619; Martinek, Tamás/0000-0003-3168-8066}
}

@article{MTMT:27695954,
	title = {Opposing Roles of FANCJ and HLTF Protect Forks and Restrain Replication during Stress},
	url = {https://m2.mtmt.hu/api/publication/27695954},
	author = {Peng, M and Cong, K and Panzarino, NJ and Nayak, S and Calvo, J and Deng, B and Zhu, LJ and Mórocz, Mónika and Hegedűs, Lili and Haracska, Lajos and Cantor, SB},
	doi = {10.1016/j.celrep.2018.08.065},
	journal-iso = {CELL REP},
	journal = {CELL REPORTS},
	volume = {24},
	unique-id = {27695954},
	issn = {2211-1247},
	abstract = {The DNA helicase FANCJ is mutated in hereditary breast and ovarian cancer and Fanconi anemia (FA). Nevertheless, how loss of FANCJ translates to disease pathogenesis remains unclear. We addressed this question by analyzing proteins associated with replication forks in cells with or without FANCJ. We demonstrate that FANCJ-knockout (FANCJ-KO) cells have alterations in the replisome that are consistent with enhanced replication stress, including an aberrant accumulation of the fork remodeling factor helicase-like transcription factor (HLTF). Correspondingly, HLTF contributes to fork degradation in FANCJ-KO cells. Unexpectedly, the unrestrained DNA synthesis that characterizes HLTF-deficient cells is FANCJ dependent and correlates with S1 nuclease sensitivity and fork degradation. These results suggest that FANCJ and HLTF promote replication fork integrity, in part by counteracting each other to keep fork remodeling and elongation in check. Indicating one protein compensates for loss of the other, loss of both HLTF and FANCJ causes a more severe replication stress response.},
	keywords = {CELLS; REPAIR; S-PHASE; Homologous recombination; DNA-DAMAGE RESPONSE; helicase; BACH1; TRANSLOCASE ACTIVITY; NASCENT DNA},
	year = {2018},
	eissn = {2211-1247},
	pages = {3251-3261}
}

@article{MTMT:3318793,
	title = {Intelligent image-based in situ single-cell isolation},
	url = {https://m2.mtmt.hu/api/publication/3318793},
	author = {Braskó, Csilla and Smith, K and Molnár, Csaba and Faragó, Nóra and Hegedűs, Lili and Bálind, Árpád and Balassa, Tamás and Szkalisity, Ábel and Sükösd, Farkas and Kocsis, Ágnes Katalin and Bálint, Balázs and Paavolainen, L and Enyedi, Márton Zsolt and Nagy, István and Puskás, László and Haracska, Lajos and Tamás, Gábor and Horváth, Péter},
	doi = {10.1038/s41467-017-02628-4},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {9},
	unique-id = {3318793},
	issn = {2041-1723},
	abstract = {Quantifying heterogeneities within cell populations is important for many fields including cancer research and neurobiology; however, techniques to isolate individual cells are limited. Here, we describe a high-throughput, non-disruptive, and cost-effective isolation method that is capable of capturing individually targeted cells using widely available techniques. Using high-resolution microscopy, laser microcapture microscopy, image analysis, and machine learning, our technology enables scalable molecular genetic analysis of single cells, targetable by morphology or location within the sample.},
	year = {2018},
	eissn = {2041-1723},
	orcid-numbers = {Molnár, Csaba/0000-0002-6124-1209; Tamás, Gábor/0000-0002-7905-6001}
}

@article{MTMT:3140736,
	title = {The DNA-binding box of human SPARTAN contributes to the targeting of Poleta to DNA damage sites.},
	url = {https://m2.mtmt.hu/api/publication/3140736},
	author = {Tóth, Ágnes and Hegedűs, Lili and Juhász, Szilvia and Haracska, Lajos and Burkovics, Péter},
	doi = {10.1016/j.dnarep.2016.10.007},
	journal-iso = {DNA REPAIR},
	journal = {DNA REPAIR},
	volume = {49},
	unique-id = {3140736},
	issn = {1568-7864},
	abstract = {Inappropriate repair of UV-induced DNA damage results in human diseases such as Xeroderma pigmentosum (XP), which is associated with an extremely high risk of skin cancer. A variant form of XP is caused by the absence of Poleta, which is normally able to bypass UV-induced DNA lesions in an error-free manner. However, Poleta is highly error prone when replicating undamaged DNA and, thus, the regulation of the proper targeting of Poleta is crucial for the prevention of mutagenesis and UV-induced cancer formation. Spartan is a novel regulator of the damage tolerance pathway, and its association with Ub-PCNA has a role in Poleta targeting; however, our knowledge about its function is only rudimentary. Here, we describe a new biochemical property of purified human SPARTAN by showing that it is a DNA-binding protein. Using a DNA binding mutant, we provide in vivo evidence that DNA binding by SPARTAN regulates the targeting of Poleta to damage sites after UV exposure, and this function contributes highly to its DNA-damage tolerance function.},
	year = {2017},
	eissn = {1568-7856},
	pages = {33-42},
	orcid-numbers = {Burkovics, Péter/0000-0001-5106-5371}
}

@misc{MTMT:3083577,
	title = {A PARI fehérje, mint a homológ rekombináció szuppresszora},
	url = {https://m2.mtmt.hu/api/publication/3083577},
	author = {Hegedűs, Lili},
	unique-id = {3083577},
	year = {2016}
}

@misc{MTMT:3083377,
	title = {Regulation of DNA damage tolerance by ZBTB1},
	url = {https://m2.mtmt.hu/api/publication/3083377},
	author = {Dudas, K and Hegedűs, Lili and Haracska, L and Burkovics, P},
	unique-id = {3083377},
	year = {2016}
}

@{MTMT:3083365,
	title = {PARI as a regulator of homologous recombination},
	url = {https://m2.mtmt.hu/api/publication/3083365},
	author = {Hegedűs, Lili and Sebesta, M and Altmannova, V and Haracska, L and Krejci, L and Burkovics, P},
	booktitle = {7th DNA Repair Workshop},
	unique-id = {3083365},
	year = {2016}
}

@CONFERENCE{MTMT:3082928,
	title = {Regulation of DNA damage tolerance by ZBTB1},
	url = {https://m2.mtmt.hu/api/publication/3082928},
	author = {Dudas, K and Hegedűs, Lili and Haracska, L and Burkovics, P},
	booktitle = {Straub-napok},
	unique-id = {3082928},
	year = {2016}
}

@CONFERENCE{MTMT:3082794,
	title = {The role of human Spartan in the maintenance of genome integrity},
	url = {https://m2.mtmt.hu/api/publication/3082794},
	author = {Zsigmond, Eszter and Morocz, M and Toth, R and Berczeli, Orsolya and Hegedűs, Lili and Juhasz, S and Haracska, L},
	booktitle = {Straub-napok},
	unique-id = {3082794},
	year = {2016}
}