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  1. Article ; Online: Under the Influence: Cas9 Ends and DNA Repair Outcomes.

    Jasin, Maria

    The CRISPR journal

    2019  Volume 1, Page(s) 132–134

    Language English
    Publishing date 2019-04-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3017891-5
    ISSN 2573-1602 ; 2573-1599
    ISSN (online) 2573-1602
    ISSN 2573-1599
    DOI 10.1089/crispr.2018.29014.jas
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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair.

    Lim, Pei Xin / Zaman, Mahdia / Feng, Weiran / Jasin, Maria

    Molecular cell

    2024  Volume 84, Issue 3, Page(s) 447–462.e10

    Abstract: Tumor suppressor BRCA2 functions in homology-directed repair (HDR), the protection of stalled replication forks, and the suppression of replicative gaps, but their relative contributions to genome integrity and chemotherapy response are under scrutiny. ... ...

    Abstract Tumor suppressor BRCA2 functions in homology-directed repair (HDR), the protection of stalled replication forks, and the suppression of replicative gaps, but their relative contributions to genome integrity and chemotherapy response are under scrutiny. Here, we report that mouse and human cells require a RAD51 filament stabilization motif in BRCA2 for fork protection and gap suppression but not HDR. In mice, the loss of fork protection/gap suppression does not compromise genome stability or shorten tumor latency. By contrast, HDR deficiency increases spontaneous and replication stress-induced chromosome aberrations and tumor predisposition. Unlike with HDR, fork protection/gap suppression defects are also observed in Brca2 heterozygous cells, likely due to reduced RAD51 stabilization at stalled forks/gaps. Gaps arise from PRIMPOL activity, which is associated with 5-hydroxymethyl-2'-deoxyuridine sensitivity due to the formation of SMUG1-generated abasic sites and is exacerbated by poly(ADP-ribose) polymerase (PARP) inhibition. However, HDR proficiency has the major role in mitigating sensitivity to chemotherapeutics, including PARP inhibitors.
    MeSH term(s) Animals ; Humans ; Mice ; BRCA2 Protein/metabolism ; DNA Repair ; DNA Replication ; Genomic Instability ; Genomics ; Rad51 Recombinase/genetics ; Rad51 Recombinase/metabolism ; Recombinational DNA Repair
    Chemical Substances BRCA2 Protein ; BRCA2 protein, human ; Rad51 Recombinase (EC 2.7.7.-)
    Language English
    Publishing date 2024-01-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2023.12.025
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  3. Article: BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair.

    Lim, Pei Xin / Zaman, Mahdia / Jasin, Maria

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Highlights: Gap suppression requires BRCA2 C-terminal RAD51 binding in mouse and human cells : Etoc blurb: Lim : Summary: Tumor suppressor BRCA2 functions in homology-directed repair (HDR), protection of stalled replication forks, and suppression ... ...

    Abstract Highlights: Gap suppression requires BRCA2 C-terminal RAD51 binding in mouse and human cells
    Etoc blurb: Lim
    Summary: Tumor suppressor BRCA2 functions in homology-directed repair (HDR), protection of stalled replication forks, and suppression of replicative gaps. The relative contributions of these pathways to genome integrity and chemotherapy response are under scrutiny. Here, we report that mouse and human cells require a RAD51 filament stabilization motif in BRCA2 for both fork protection and gap suppression, but not HDR. Loss of fork protection and gap suppression do not compromise genome instability or shorten tumor latency in mice or cause replication stress in human mammary cells. By contrast, HDR deficiency increases spontaneous and replication stress-induced chromosome aberrations and tumor predisposition. Unlike with HDR, fork protection and gap suppression defects are also observed in
    Language English
    Publishing date 2023-04-11
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.11.536470
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Repair-seq: Seeking and Perturbing DNA Repair.

    Medhi, Darpan / Jasin, Maria

    The CRISPR journal

    2021  Volume 4, Issue 6, Page(s) 773–775

    MeSH term(s) CRISPR-Cas Systems ; DNA Damage ; DNA Repair/genetics ; Gene Editing
    Language English
    Publishing date 2021-12-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3017891-5
    ISSN 2573-1602 ; 2573-1599
    ISSN (online) 2573-1602
    ISSN 2573-1599
    DOI 10.1089/crispr.2021.29140.dme
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  5. Article ; Online: CRISPR at lightning speeds.

    Medhi, Darpan / Jasin, Maria

    Science (New York, N.Y.)

    2020  Volume 368, Issue 6496, Page(s) 1180–1181

    MeSH term(s) Clustered Regularly Interspaced Short Palindromic Repeats
    Language English
    Publishing date 2020-11-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abc3997
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  6. Article ; Online: Accolades for the DNA Damage Response.

    Jasin, Maria

    The New England journal of medicine

    2015  Volume 373, Issue 16, Page(s) 1492–1495

    MeSH term(s) Awards and Prizes ; Bacteria/genetics ; Bacteriology/history ; Biomedical Research/history ; DNA Damage/physiology ; DNA Repair/physiology ; Eukaryota/genetics ; Genetics/history ; History, 20th Century ; History, 21st Century ; Humans ; Mutation ; United States
    Language English
    Publishing date 2015-10-15
    Publishing country United States
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMp1509698
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  7. Article ; Online: De novo deletions and duplications at recombination hotspots in mouse germlines.

    Lukaszewicz, Agnieszka / Lange, Julian / Keeney, Scott / Jasin, Maria

    Cell

    2021  Volume 184, Issue 24, Page(s) 5970–5984.e18

    Abstract: Numerous DNA double-strand breaks (DSBs) arise during meiosis to initiate homologous recombination. These DSBs are usually repaired faithfully, but here, we uncover a distinct type of mutational event in which deletions form via joining of ends from two ... ...

    Abstract Numerous DNA double-strand breaks (DSBs) arise during meiosis to initiate homologous recombination. These DSBs are usually repaired faithfully, but here, we uncover a distinct type of mutational event in which deletions form via joining of ends from two closely spaced DSBs (double cuts) within a single hotspot or at adjacent hotspots on the same or different chromatids. Deletions occur in normal meiosis but are much more frequent when DSB formation is dysregulated in the absence of the ATM kinase. Events between chromosome homologs point to multi-chromatid damage and aborted gap repair. Some deletions contain DNA from other hotspots, indicating that double cutting at distant sites creates substrates for insertional mutagenesis. End joining at double cuts can also yield tandem duplications or extrachromosomal circles. Our findings highlight the importance of DSB regulation and reveal a previously hidden potential for meiotic mutagenesis that is likely to affect human health and genome evolution.
    MeSH term(s) Animals ; Ataxia Telangiectasia Mutated Proteins/deficiency ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Base Sequence ; Chromatids/metabolism ; Chromosomes, Mammalian/genetics ; Crosses, Genetic ; DNA Breaks, Double-Stranded ; DNA, Circular/genetics ; Female ; Gene Deletion ; Gene Duplication ; Genome ; Germ Cells/metabolism ; Haplotypes/genetics ; Homologous Recombination/genetics ; Male ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mutagenesis, Insertional/genetics ; Mutation/genetics ; Recombination, Genetic/genetics ; Mice
    Chemical Substances DNA, Circular ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1)
    Language English
    Publishing date 2021-11-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.10.025
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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  8. Article ; Online: Homologous Recombination and Replication Fork Protection: BRCA2 and More!

    Feng, Weiran / Jasin, Maria

    Cold Spring Harbor symposia on quantitative biology

    2018  Volume 82, Page(s) 329–338

    Abstract: BRCA2 is a breast and ovarian tumor suppressor that guards against genome instability, a hallmark of cancer. Significant progress has been made in improving our understanding of BRCA2 function from biochemical, cellular, and mouse studies. The knowledge ... ...

    Abstract BRCA2 is a breast and ovarian tumor suppressor that guards against genome instability, a hallmark of cancer. Significant progress has been made in improving our understanding of BRCA2 function from biochemical, cellular, and mouse studies. The knowledge gained has been actively exploited to develop therapeutic strategies, including PARP inhibition, which has shown promising clinical outcomes. Recently, tremendous excitement has been generated by the findings of the roles of BRCA2 and other proteins in suppressing replication stress through homologous recombination and in the protection of stalled replication forks. Processes such as mitotic DNA synthesis and fork reversal have taken center stage in these studies. Here, we discuss our recent findings in the context of these advances.
    Language English
    Publishing date 2018-04-23
    Publishing country United States
    Document type Journal Article
    ISSN 1943-4456 ; 0091-7451
    ISSN (online) 1943-4456
    ISSN 0091-7451
    DOI 10.1101/sqb.2017.82.035006
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  9. Article: Induction of Chromosomal Translocations with CRISPR-Cas9 and Other Nucleases: Understanding the Repair Mechanisms That Give Rise to Translocations.

    Brunet, Erika / Jasin, Maria

    Advances in experimental medicine and biology

    2018  Volume 1044, Page(s) 15–25

    Abstract: Chromosomal translocations are associated with several tumor types, including hematopoietic malignancies, sarcomas, and solid tumors of epithelial origin, due to their activation of a proto-oncogene or generation of a novel fusion protein with oncogenic ... ...

    Abstract Chromosomal translocations are associated with several tumor types, including hematopoietic malignancies, sarcomas, and solid tumors of epithelial origin, due to their activation of a proto-oncogene or generation of a novel fusion protein with oncogenic potential. In many cases, the availability of suitable human models has been lacking because of the difficulty in recapitulating precise expression of the fusion protein or other reasons. Further, understanding how translocations form mechanistically has been a goal, as it may suggest ways to prevent their occurrence. Chromosomal translocations arise when DNA ends from double-strand breaks (DSBs) on two heterologous chromosomes are improperly joined. This review provides a summary of DSB repair mechanisms and their contribution to translocation formation, the various programmable nuclease platforms that have been used to generate translocations, and the successes that have been achieved in this area.
    MeSH term(s) Animals ; CRISPR-Cas Systems ; DNA Breaks, Double-Stranded ; DNA Repair ; Endonucleases ; Humans ; Mice ; Translocation, Genetic
    Chemical Substances Endonucleases (EC 3.1.-)
    Language English
    Publishing date 2018-05-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-981-13-0593-1_2
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  10. Article ; Online: Mechanistic Insight into Crossing over during Mouse Meiosis.

    Peterson, Shaun E / Keeney, Scott / Jasin, Maria

    Molecular cell

    2020  Volume 78, Issue 6, Page(s) 1252–1263.e3

    Abstract: Crossover recombination is critical for meiotic chromosome segregation, but how mammalian crossing over is accomplished is poorly understood. Here, we illuminate how strands exchange during meiotic recombination in male mice by analyzing patterns of ... ...

    Abstract Crossover recombination is critical for meiotic chromosome segregation, but how mammalian crossing over is accomplished is poorly understood. Here, we illuminate how strands exchange during meiotic recombination in male mice by analyzing patterns of heteroduplex DNA in recombinant molecules preserved by the mismatch correction deficiency of Msh2
    MeSH term(s) Animals ; Chromosome Segregation/genetics ; Crossing Over, Genetic/genetics ; Crossing Over, Genetic/physiology ; DNA Breaks, Double-Stranded ; DNA Repair/genetics ; DNA, Cruciform/genetics ; DNA, Cruciform/metabolism ; Homologous Recombination/genetics ; Homologous Recombination/physiology ; Male ; Meiosis/genetics ; Meiosis/physiology ; Mice ; Mice, Inbred DBA ; MutS Homolog 2 Protein/genetics ; MutS Homolog 2 Protein/metabolism ; Nucleic Acid Heteroduplexes/genetics
    Chemical Substances DNA, Cruciform ; Nucleic Acid Heteroduplexes ; Msh2 protein, mouse (EC 3.6.1.3) ; MutS Homolog 2 Protein (EC 3.6.1.3)
    Language English
    Publishing date 2020-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2020.04.009
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