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  1. Article ; Online: Understanding the Histone DNA Repair Code: H4K20me2 Makes Its Mark.

    Paquin, Karissa L / Howlett, Niall G

    Molecular cancer research : MCR

    2018  Volume 16, Issue 9, Page(s) 1335–1345

    Abstract: Chromatin is a highly compact structure that must be rapidly rearranged in order for DNA repair proteins to access sites of damage and facilitate timely and efficient repair. Chromatin plasticity is achieved through multiple processes, including the ... ...

    Abstract Chromatin is a highly compact structure that must be rapidly rearranged in order for DNA repair proteins to access sites of damage and facilitate timely and efficient repair. Chromatin plasticity is achieved through multiple processes, including the posttranslational modification of histone tails. In recent years, the impact of histone posttranslational modification on the DNA damage response has become increasingly well recognized, and chromatin plasticity has been firmly linked to efficient DNA repair. One particularly important histone posttranslational modification process is methylation. Here, we focus on the regulation and function of H4K20 methylation (H4K20me) in the DNA damage response and describe the writers, erasers, and readers of this important chromatin mark as well as the combinatorial histone posttranslational modifications that modulate H4K20me recognition. Finally, we discuss the central role of H4K20me in determining if DNA double-strand breaks (DSB) are repaired by the error-prone, nonhomologous DNA end joining pathway or the error-free, homologous recombination pathway. This review article discusses the regulation and function of H4K20me2 in DNA DSB repair and outlines the components and modifications that modulate this important chromatin mark and its fundamental impact on DSB repair pathway choice.
    MeSH term(s) Chromatin/genetics ; Chromatin/metabolism ; DNA Repair ; Histones/genetics ; Histones/metabolism ; Humans ; Phosphorylation
    Chemical Substances Chromatin ; Histones
    Language English
    Publishing date 2018-06-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-17-0688
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  2. Article ; Online: RI-INBRE: A Statewide NIH Program Grant to Improve Institutional Biomedical Research Capacity in Rhode Island.

    Hemme, Christopher L / Bellavia, Laura / Cho, Bongsup P / Meenach, Samantha / Howlett, Niall G

    Rhode Island medical journal (2013)

    2021  Volume 104, Issue 2, Page(s) 25–29

    Abstract: The overarching goal of the Rhode Island-IDeA Network of Biomedical Research Excellence (RI-INBRE) is to improve institutional capacity for biomedical research excellence and expand student experiential training opportunities in the State of Rhode Island. ...

    Abstract The overarching goal of the Rhode Island-IDeA Network of Biomedical Research Excellence (RI-INBRE) is to improve institutional capacity for biomedical research excellence and expand student experiential training opportunities in the State of Rhode Island. RI-INBRE comprises five major core components: The Administrative Core, the Bioinformatics Core, the Centralized Research Core Facility, the Training Core, and the Developmental Research Project Program Core. Since its inception in 2001, RI-INBRE has made significant investments and marked advancements in the biomedical research infrastructure of Rhode Island. RI-INBRE funding has increased the scale and quality of faculty research and engaged undergraduate students, graduate students, and postdoctoral fellows in structured and mentored research training experiences. Over the last 19 years, RI-INBRE has supported 212 faculty researchers and over 533 projects and has provided research-training opportunities for nearly 2,000 students, resulting in 757 publications. Through its student-training program, RI-INBRE has contributed to regional workforce development by engaging students and encouraging them to pursue careers in biomedical fields. Many of these students have been admitted to graduate or medical schools and obtained biomedical industry jobs following graduation. RI-INBRE has been particularly influential in building the research infrastructure at primarily undergraduate institutions, which have seen significant improvements in research quality and output, student training, and research infrastructure.
    MeSH term(s) Biomedical Research ; Humans ; Mentors ; Rhode Island ; Schools, Medical ; Students
    Language English
    Publishing date 2021-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 419430-5
    ISSN 2327-2228 ; 0363-7913
    ISSN (online) 2327-2228
    ISSN 0363-7913
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  3. Article: Application of a Biphasic Mathematical Model of Cancer Cell Drug Response for Formulating Potent and Synergistic Targeted Drug Combinations to Triple Negative Breast Cancer Cells.

    Shen, Jinyan / Li, Li / Howlett, Niall G / Cohen, Paul S / Sun, Gongqin

    Cancers

    2020  Volume 12, Issue 5

    Abstract: Triple negative breast cancer is a collection of heterogeneous breast cancers that are immunohistochemically negative for estrogen receptor, progesterone receptor, and ErbB2 (due to deletion or lack of amplification). No dominant proliferative driver has ...

    Abstract Triple negative breast cancer is a collection of heterogeneous breast cancers that are immunohistochemically negative for estrogen receptor, progesterone receptor, and ErbB2 (due to deletion or lack of amplification). No dominant proliferative driver has been identified for this type of cancer, and effective targeted therapy is lacking. In this study, we hypothesized that triple negative breast cancer cells are multi-driver cancer cells, and evaluated a biphasic mathematical model for identifying potent and synergistic drug combinations for multi-driver cancer cells. The responses of two triple negative breast cancer cell lines, MDA-MB-231 and MDA-MB-468, to a panel of targeted therapy drugs were determined over a broad range of concentrations. The analyses of the drug responses by the biphasic mathematical model revealed that both cell lines were indeed dependent on multiple drivers, and inhibitors of individual drivers caused a biphasic response: a target-specific partial inhibition at low nM concentrations, and an off-target toxicity at μM concentrations. We further demonstrated that combinations of drugs, targeting each driver, cause potent, synergistic, and cell-specific cell killing. Immunoblotting analysis of the effects of the individual drugs and drug combinations on the signaling pathways supports the above conclusion. These results support a multi-driver proliferation hypothesis for these triple negative breast cancer cells, and demonstrate the applicability of the biphasic mathematical model for identifying effective and synergistic targeted drug combinations for triple negative breast cancer cells.
    Language English
    Publishing date 2020-04-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12051087
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  4. Article ; Online: A distinct role for recombination repair factors in an early cellular response to transcription-replication conflicts.

    Shao, Xin / Joergensen, Amalie M / Howlett, Niall G / Lisby, Michael / Oestergaard, Vibe H

    Nucleic acids research

    2020  Volume 48, Issue 10, Page(s) 5467–5484

    Abstract: Transcription-replication (T-R) conflicts are profound threats to genome integrity. However, whilst much is known about the existence of T-R conflicts, our understanding of the genetic and temporal nature of how cells respond to them is poorly ... ...

    Abstract Transcription-replication (T-R) conflicts are profound threats to genome integrity. However, whilst much is known about the existence of T-R conflicts, our understanding of the genetic and temporal nature of how cells respond to them is poorly established. Here, we address this by characterizing the early cellular response to transient T-R conflicts (TRe). This response specifically requires the DNA recombination repair proteins BLM and BRCA2 as well as a non-canonical monoubiquitylation-independent function of FANCD2. A hallmark of the TRe response is the rapid co-localization of these three DNA repair factors at sites of T-R collisions. We find that the TRe response relies on basal activity of the ATR kinase, yet it does not lead to hyperactivation of this key checkpoint protein. Furthermore, specific abrogation of the TRe response leads to DNA damage in mitosis, and promotes chromosome instability and cell death. Collectively our findings identify a new role for these well-established tumor suppressor proteins at an early stage of the cellular response to conflicts between DNA transcription and replication.
    MeSH term(s) Ataxia Telangiectasia Mutated Proteins/metabolism ; BRCA2 Protein/physiology ; Cell Line ; Cell Survival ; Cyclin-Dependent Kinase 9/metabolism ; DNA/metabolism ; DNA Damage ; DNA Replication ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Fanconi Anemia Complementation Group D2 Protein/physiology ; Humans ; Mitosis/genetics ; Promoter Regions, Genetic ; RNA/metabolism ; RNA Polymerase II/metabolism ; RNA Splicing ; RecQ Helicases/physiology ; Recombinational DNA Repair ; Transcription, Genetic ; Ubiquitination
    Chemical Substances BRCA2 Protein ; Fanconi Anemia Complementation Group D2 Protein ; RNA (63231-63-0) ; DNA (9007-49-2) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Cyclin-Dependent Kinase 9 (EC 2.7.11.22) ; RNA Polymerase II (EC 2.7.7.-) ; Bloom syndrome protein (EC 3.6.1.-) ; RecQ Helicases (EC 3.6.4.12)
    Language English
    Publishing date 2020-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkaa268
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1067: Show issues Location:
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  5. Article ; Online: The Fanconi anemia ID2 complex: dueling saxes at the crossroads.

    Boisvert, Rebecca A / Howlett, Niall G

    Cell cycle (Georgetown, Tex.)

    2014  Volume 13, Issue 19, Page(s) 2999–3015

    Abstract: Fanconi anemia (FA) is a rare recessive genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility in early adulthood. FA is caused by biallelic germ-line mutation of any one of 16 genes. While ... ...

    Abstract Fanconi anemia (FA) is a rare recessive genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility in early adulthood. FA is caused by biallelic germ-line mutation of any one of 16 genes. While several functions for the FA proteins have been ascribed, the prevailing hypothesis is that the FA proteins function cooperatively in the FA-BRCA pathway to repair damaged DNA. A pivotal step in the activation of the FA-BRCA pathway is the monoubiquitination of the FANCD2 and FANCI proteins. Despite their importance for DNA repair, the domain structure, regulation, and function of FANCD2 and FANCI remain poorly understood. In this review, we provide an overview of our current understanding of FANCD2 and FANCI, with an emphasis on their posttranslational modification and common and unique functions.
    MeSH term(s) DNA/chemistry ; DNA/metabolism ; DNA Repair ; Fanconi Anemia/metabolism ; Fanconi Anemia/pathology ; Fanconi Anemia Complementation Group D2 Protein/chemistry ; Fanconi Anemia Complementation Group D2 Protein/genetics ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Fanconi Anemia Complementation Group Proteins/chemistry ; Fanconi Anemia Complementation Group Proteins/genetics ; Fanconi Anemia Complementation Group Proteins/metabolism ; Humans ; Nucleosomes/metabolism ; Protein Processing, Post-Translational ; Protein Structure, Tertiary
    Chemical Substances FANCI protein, human ; Fanconi Anemia Complementation Group D2 Protein ; Fanconi Anemia Complementation Group Proteins ; Nucleosomes ; DNA (9007-49-2)
    Language English
    Publishing date 2014-12-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/15384101.2014.956475
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  6. Article: Differential Regulation of Retinoic Acid Metabolism in Fanconi Anemia.

    Blaize, Justin L / Noori, Bahaa M / Hunter, Kelsey P / Henrikson, Kathryn A / Atoyan, Janet A / Ardito, Alan A / Donovan, Frank X / Chandrasekharappa, Settara C / Schindler, Detlev / Howlett, Niall G

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Fanconi anemia (FA) is a rare genetic disease characterized by heterogeneous congenital abnormalities and increased risk for bone marrow failure and cancer. FA is caused by mutation of any one of 23 genes, the protein products of which function primarily ...

    Abstract Fanconi anemia (FA) is a rare genetic disease characterized by heterogeneous congenital abnormalities and increased risk for bone marrow failure and cancer. FA is caused by mutation of any one of 23 genes, the protein products of which function primarily in the maintenance of genome stability. An important role for the FA proteins in the repair of DNA interstrand crosslinks (ICLs) has been established
    Language English
    Publishing date 2023-04-27
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.06.535759
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  7. Article: Fanconi anemia: Fanconi anemia, breast and embryonal cancer risk revisited.

    Howlett, Niall G

    European journal of human genetics : EJHG

    2007  Volume 15, Issue 7, Page(s) 715–717

    MeSH term(s) Breast Neoplasms/genetics ; Child ; DNA Repair ; Fanconi Anemia/genetics ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Fanconi Anemia Complementation Group N Protein ; Humans ; Metabolic Networks and Pathways ; Models, Biological ; Neoplasms, Germ Cell and Embryonal/etiology ; Neoplasms, Germ Cell and Embryonal/genetics ; Nuclear Proteins/genetics ; Risk ; Tumor Suppressor Proteins/genetics
    Chemical Substances FANCD2 protein, human ; Fanconi Anemia Complementation Group D2 Protein ; Fanconi Anemia Complementation Group N Protein ; Nuclear Proteins ; PALB2 protein, human ; Tumor Suppressor Proteins
    Language English
    Publishing date 2007-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 1141470-4
    ISSN 1476-5438 ; 1018-4813
    ISSN (online) 1476-5438
    ISSN 1018-4813
    DOI 10.1038/sj.ejhg.5201860
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  8. Article ; Online: A DUB-less step? Tighten up D-loop.

    Paquin, Karissa L / Vierra, David A / Howlett, Niall G

    Cell cycle (Georgetown, Tex.)

    2016  Volume 15, Issue 23, Page(s) 3163–3164

    MeSH term(s) DNA Repair ; Fanconi Anemia ; Fanconi Anemia Complementation Group D2 Protein/genetics ; Fanconi Anemia Complementation Group Proteins/genetics
    Chemical Substances Fanconi Anemia Complementation Group D2 Protein ; Fanconi Anemia Complementation Group Proteins
    Language English
    Publishing date 2016-09-14
    Publishing country United States
    Document type News ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2016.1226603
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  9. Article ; Online: Recent discoveries in the molecular pathogenesis of the inherited bone marrow failure syndrome Fanconi anemia.

    Mamrak, Nicholas E / Shimamura, Akiko / Howlett, Niall G

    Blood reviews

    2016  Volume 31, Issue 3, Page(s) 93–99

    Abstract: Fanconi anemia (FA) is a rare autosomal and X-linked genetic disease characterized by congenital abnormalities, progressive bone marrow failure (BMF), and increased cancer risk during early adulthood. The median lifespan for FA patients is approximately ... ...

    Abstract Fanconi anemia (FA) is a rare autosomal and X-linked genetic disease characterized by congenital abnormalities, progressive bone marrow failure (BMF), and increased cancer risk during early adulthood. The median lifespan for FA patients is approximately 33years. The proteins encoded by the FA genes function together in the FA-BRCA pathway to repair DNA damage and to maintain genome stability. Within the past two years, five new FA genes have been identified-RAD51/FANCR, BRCA1/FANCS, UBE2T/FANCT, XRCC2/FANCU, and REV7/FANCV-bringing the total number of disease-causing genes to 21. This review summarizes the discovery of these new FA genes and describes how these proteins integrate into the FA-BRCA pathway to maintain genome stability and critically prevent early-onset BMF and cancer.
    MeSH term(s) BRCA1 Protein/genetics ; BRCA1 Protein/metabolism ; Bone Marrow/metabolism ; Bone Marrow/pathology ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Fanconi Anemia/etiology ; Fanconi Anemia/metabolism ; Fanconi Anemia/pathology ; Fanconi Anemia Complementation Group Proteins/genetics ; Fanconi Anemia Complementation Group Proteins/metabolism ; Genomic Instability ; Homologous Recombination ; Humans ; Mad2 Proteins/genetics ; Mad2 Proteins/metabolism ; Mutation ; Rad51 Recombinase/genetics ; Rad51 Recombinase/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Conjugating Enzymes/genetics ; Ubiquitin-Conjugating Enzymes/metabolism
    Chemical Substances BRCA1 Protein ; BRCA1 protein, human ; DNA-Binding Proteins ; Fanconi Anemia Complementation Group Proteins ; MAD2L2 protein, human ; Mad2 Proteins ; Ubiquitin ; XRCC2 protein, human ; UBE2T protein, human (EC 2.3.2.23) ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23) ; Rad51 Recombinase (EC 2.7.7.-)
    Language English
    Publishing date 2016-10-13
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 639015-8
    ISSN 1532-1681 ; 0268-960X
    ISSN (online) 1532-1681
    ISSN 0268-960X
    DOI 10.1016/j.blre.2016.10.002
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  10. Article ; Online: FANCP/SLX4: a Swiss army knife of DNA interstrand crosslink repair.

    Cybulski, Kelly E / Howlett, Niall G

    Cell cycle (Georgetown, Tex.)

    2011  Volume 10, Issue 11, Page(s) 1757–1763

    Abstract: Fanconi anemia (FA) is a rare genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility. The FA proteins are known to function in the cellular defense against DNA interstrand crosslinks (ICLs), a ... ...

    Abstract Fanconi anemia (FA) is a rare genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility. The FA proteins are known to function in the cellular defense against DNA interstrand crosslinks (ICLs), a process that remains poorly understood. A recent spate of discoveries has led to the identification of one new FA gene, FANCP/SLX4, and two strong candidate FA genes, FAN1 and RAD51C. In this perspective we describe the discovery of FANCP/SLX4 and discuss how these new findings collectively refine our understanding of DNA ICL repair.
    MeSH term(s) DNA Repair ; Fanconi Anemia/genetics ; Fanconi Anemia Complementation Group Proteins/genetics ; Humans ; Recombinases/genetics
    Chemical Substances Fanconi Anemia Complementation Group Proteins ; Recombinases ; SLX4 protein, human (EC 3.1.-)
    Language English
    Publishing date 2011-06-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.10.11.15818
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