Search Results - "Bralić, Amer"

Resolution of the Holliday junction recombination intermediate by human GEN1 at the single-molecule level by Sobhy, Mohamed A, Bralić, Amer, Raducanu, Vlad-Stefan, Takahashi, Masateru, Tehseen, Muhammad, Rashid, Fahad, Zaher, Manal S, Hamdan, Samir M

“…Abstract Human GEN1 is a cytosolic homologous recombination protein that resolves persisting four-way Holliday junctions (HJ) after the dissolution of the…”
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Envisioning how the prototypic molecular machine TFIIH functions in transcription initiation and DNA repair by Tsutakawa, Susan E., Tsai, Chi-Lin, Yan, Chunli, Bralić, Amer, Chazin, Walter J., Hamdan, Samir M., Schärer, Orlando D., Ivanov, Ivaylo, Tainer, John A.

“…Critical for transcription initiation and bulky lesion DNA repair, TFIIH provides an exemplary system to connect molecular mechanisms to biological outcomes…”
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A scanning-to-incision switch in TFIIH-XPG induced by DNA damage licenses nucleotide excision repair by Bralić, Amer, Tehseen, Muhammad, Sobhy, Mohamed A, Tsai, Chi-Lin, Alhudhali, Lubna, Yi, Gang, Yu, Jina, Yan, Chunli, Ivanov, Ivaylo, Tsutakawa, Susan E, Tainer, John A, Hamdan, Samir M

“…Nucleotide excision repair (NER) is critical for removing bulky DNA base lesions and avoiding diseases. NER couples lesion recognition by XPC to strand…”
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Implementing fluorescence enhancement, quenching, and FRET for investigating flap endonuclease 1 enzymatic reaction at the single-molecule level by Sobhy, Mohamed A., Tehseen, Muhammad, Takahashi, Masateru, Bralić, Amer, De Biasio, Alfredo, Hamdan, Samir M.

“…[Display omitted] Flap endonuclease 1 (FEN1) is an important component of the intricate molecular machinery for DNA replication and repair. FEN1 is a…”
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Decoding Cancer Variants of Unknown Significance for Helicase-Nuclease-RPA Complexes Orchestrating DNA Repair During Transcription and Replication by Tsutakawa, Susan E, Bacolla, Albino, Katsonis, Panagiotis, Bralić, Amer, Hamdan, Samir M, Lichtarge, Olivier, Tainer, John A, Tsai, Chi-Lin

“…All tumors have DNA mutations, and a predictive understanding of those mutations could inform clinical treatments. However, 40% of the mutations are variants…”
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