Nabieh  Ayoub

Nabieh Ayoub

Education/ Resume:

PhD, 2004, Hadassah Medical School, The Hebrew University of Jerusalem.
MSc, 1997, Givaat-Ram, The Hebrew University of Jerusalem.
BSc, 1994, Givaat-Ram, The Hebrew University of Jerusalem.

Research Summary

Each cell in our body could experience tens of thousands of DNA lesions per day. Fortunately, cells have evolved a sophisticated network of cellular mechanisms, termed the DNA damage response (DDR), to detect DNA lesions and facilitate their repair. Defective DDR could lead to accumulation of mutations and genomic instabilities that contribute to premature aging, developmental disorders, neurodegenerative disease and cancer.

Our lab is interested in understanding how cells repair broken DNA. We focus on identifying new DDR proteins, characterizing their role in DNA damage repair and cancer development. Our ultimate goal is to translate our discoveries into diagnostic and personalized therapeutic tools to defeat cancer and other related diseases.

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  • Research Committee member of the Israel Cancer Association, 2020
  • Excellence research scholarship from the Israel Cancer Association, 2020
  • Yanai Prize for Excellence in Academic Education, 2019
  • Technion-Distinguished Lecturer, 2017
  • Maaof fellowship for outstanding Arab lecturers, 2009-2012
  • Senior Investigator Scientist- tenured position at the MRC, Cambridge, UK, 2008.
  • International Agency for Research on Cancer award, 2003.
  • AAAS Newcomb Cleveland Prize for an outstanding contribution to science, 2003.
  • Levy Eshkol fellowship from the Israeli Ministry of Science, 2001.
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Key Publications
  • Harnessing DNA replication stress to target RBM10 deficiency in lung adenocarcinoma.
    Machour, F. E., Abu-Zhayia, E., Kamar, J., Barisaac, A. S., Simon, I., and Ayoub, N. bioRxiv, 2023. 
  • A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.
    Ben-Oz, B. M., Machour, F. E., Nicola, M., Argoetti, A., Polyak, G., Hanna, R., Kleifeld, O., Mandel-Gutfreund, Y., and Ayoub, N. Nature communications 14, 7628 (2023).
    PMID: 37993446; DOI: 10.1038/s41467-023-43495-6
  • Recruitment of RBM6 to DNA Double-Strand Breaks Fosters Homologous Recombination Repair.
    Awwad, S. W., Darawshe, M. M., Machour, F. E., Arman, I., and Ayoub, N. Mol Cell Biol 43, 130-142 (2023).
    PMID: 36941773; DOI: 10.1080/10985549.2023.2187105
  • Selective macrocyclic peptide modulators of Lys63-linked ubiquitin chains disrupt DNA damage repair.
    Vamisetti, G. B., Saha, A., Huang, Y. J., Vanjari, R., Mann, G., Gutbrod, J., Ayoub, N., Suga, H., and Brik, A. Nature communications 13, 6174 (2022).
    PMID: 36257952; DOI: 10.1038/s41467-022-33808-6
  • CDYL1-dependent decrease in lysine crotonylation at DNA double-strand break sites functionally uncouples transcriptional silencing and repair.
    Abu-Zhayia, E.R., Bishara, L.A., Machour, F.E., Barisaac, A.S., Ben-Oz, B.M., and Ayoub, N.  Mol Cell. 82, 1940-1955 e1947 (2022).
    PMID: 35447080; DOI: 10.1016/j.molcel.2022.03.031
  • RBM6 splicing factor promotes homologous recombination repair of double-strand breaks and modulates sensitivity to chemotherapeutic drugs. Machour, F.E., Abu-Zhayia, E.R., Awwad, S.W., Bidany-Mizrahi, T., Meinke, S., Bishara, L.A., Heyd, F., Aqeilan, R.I., and Ayoub, N.  Nucleic Acids Res. 49, 11708-11727 (2021).
    PMID: 34718714; DOI: 10.1093/nar/gkab976
  • Transcriptional Regulation at DSBs: Mechanisms and Consequences. Machour, F.E., and Ayoub, N. Trends Genet 36, 981-997 (2020).
  • PMID: 32001024; doi: 1016/j.tig.2020.01.001
  • NELF complex fosters BRCA1 and RAD51 recruitment to DNA damage sites and modulates sensitivity to PARP inhibition. Bishara, L.A., Machour, F.E., Awwad, S.W., and Ayoub, N. DNA Repair (Amst) 97, 103025 (2020).
  • PMID: 33248388; doi:1016/j.dnarep.2020.103025
  • HDAC-dependent decrease in histone crotonylation during DNA damage. Abu-Zhayia, E.R., Machour, F.E., and Ayoub, N.. J Mol Cell Biol 11, 804-806 (2019).
  • PMID: 30864665; doi: 1093/jmcb/mjz019
  • CDYL1 fosters double-strand break-induced transcription silencing and promotes homology-directed repair. Abu-Zhaiya ER, Awwad SW, Khoury-Haddad H, Ben-OZ B, Ayoub N. J Mol Cell Biol 10, 341-357 (2018).
  • PMID: 29177481; doi: 1093/jmcb/mjx050
  • NELF-E is recruited to DNA double-strand break sites to promote transcription repression and repair. Awwad SW, Abu-Zhaiya ER, Guttmann-Raviv, N. Ayoub N. EMBO Rep.;18:745-64 (2017).
  • PMID: 28336775; doi: 15252/embr.201643191 
  • RNA-dependent chromatin localization of KDM4D lysine demethylase promotes H3K9me3 demethylation. Zoabi M, Nadar-Ponniah PT, Khoury-Haddad H, Usaj M, Budowski-Tal I, Haran T, Henn A, Mandel-Gutfreund Y, Ayoub N. Nucleic Acids Res 42:13026-38 (2014).
  • PMID: 25378304; doi:1093/nar/gku1021
  • KDM4C (GASC1) lysine demethylase is associated with mitotic chromatin and regulates chromosome segregation during mitosis. Kupershmit, I., Khoury-Haddad, H., Awwad, S.W., Guttmann-Raviv, N. and Ayoub, N. Nucleic Acids Res. 42:6168-6182 (2014).
  • PMID: 24728997; doi:1093/nar/gku253 
  • PARP1-dependent recruitment of KDM4D histone demethylase to DNA damage sites promotes double-strand break repair. Khoury-Haddad, H., Guttmann-Raviv, N., Ipenberg, I., Huggins, D., Jeyasekharan, A.D. and Ayoub, N. PNAS Plus, 111, E728-737 (2014).
  • PMID: 24550317; doi: 1073/pnas.1317585111
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Open Positions

 Excellent & motivated MSC/PhD students are invited to apply to take part in challenging projects that focus on identifying novel DNA repair proteins and exploiting them for developing innovative targeted therapeutic strategies for cancer patients. This project involves a broad range of cutting-edge techniques including advanced live-cell microscopy, CRISPR-Cas9 screen, bioinformatic analysis, and cancer xenograft mouse model.

Please send your application with a CV to:

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