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  1. AU="Bishop, A J R"
  2. AU=Sueda Taijiro
  3. AU="Helliwell, Alexandra"
  4. AU="Pitman, Roger K"
  5. AU="España-Sanchez, Beatriz Liliana"
  6. AU="Deibel, C M"
  7. AU="Duarte, Aires"
  8. AU="Man Hong"
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  1. Article ; Online: RLSuite: An Integrative R-Loop Bioinformatics Framework.

    Miller, H E / Montemayor, D / Levy, S / Sharma, K / Frost, B / Bishop, A J R

    Journal of bioinformatics and systems biology : Open access

    2023  Volume 6, Issue 4, Page(s) 364–378

    Abstract: We recently described the development of a database of 810 R-loop mapping datasets and used this data to conduct a meta-analysis of R-loops. R-loops are three-stranded nucleic acid structures containing RNA:DNA hybrids and we were able to verify that 30% ...

    Abstract We recently described the development of a database of 810 R-loop mapping datasets and used this data to conduct a meta-analysis of R-loops. R-loops are three-stranded nucleic acid structures containing RNA:DNA hybrids and we were able to verify that 30% of expressed genes have an associated R-loop in a location conserved manner.. Moreover, intergenic R-loops map to enhancers, super enhancers and with TAD domain boundaries. This work demonstrated that R-loop mapping via high-throughput sequencing can reveal novel insight into R-loop biology, however the analysis and quality control of these data is a non-trivial task for which few bioinformatic tools exist. Herein we describe RLSuite, an integrative R-loop bioinformatics framework for pre-processing, quality control, and downstream analysis of R-loop mapping data. RLSuite enables users to compare their data to hundreds of public datasets and generate a user-friendly analysis report for sharing with non-bioinformatician colleagues. Taken together, RLSuite is a novel analysis framework that should greatly benefit the emerging R-loop bioinformatics community in a rapidly expanding aspect of epigenetic control that is still poorly understood.
    Language English
    Publishing date 2023-12-21
    Publishing country United States
    Document type Journal Article
    ISSN 2688-5107
    ISSN (online) 2688-5107
    DOI 10.26502/jbsb.5107071
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Minisatellite variants generated in yeast meiosis involve DNA removal during gene conversion

    Bishop, A.J.R / Louis, E.J / Borts, R.H

    Genetics. Sept 2000. v. 156 (1)

    2000  

    Keywords Saccharomyces cerevisiae ; gene conversion ; meiosis ; microsatellite repeats ; alleles ; DNA ; loci ; nucleotide sequences ; genetic markers ; genetic recombination ; mutation
    Language English
    Dates of publication 2000-09
    Size p. 7-20.
    Document type Article
    ZDB-ID 2167-2
    ISSN 1943-2631 ; 0016-6731
    ISSN (online) 1943-2631
    ISSN 0016-6731
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 49/90: Show issues

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  3. Article: p21 controls patterning but not homologous recombination in RPE development.

    Bishop, A J R / Kosaras, B / Hollander, M C / Fornace, A / Sidman, R L / Schiestl, R H

    DNA repair

    2006  Volume 5, Issue 1, Page(s) 111–120

    Abstract: p21/WAF1/CIP1/MDA6 is a key cell cycle regulator. Cell cycle regulation is an important part of development, differentiation, DNA repair and apoptosis. Following DNA damage, p53 dependent expression of p21 results in a rapid cell cycle arrest. p21 also ... ...

    Abstract p21/WAF1/CIP1/MDA6 is a key cell cycle regulator. Cell cycle regulation is an important part of development, differentiation, DNA repair and apoptosis. Following DNA damage, p53 dependent expression of p21 results in a rapid cell cycle arrest. p21 also appears to be important for the development of melanocytes, promoting their differentiation and melanogenesis. Here, we examine the effect of p21 deficiency on the development of another pigmented tissue, the retinal pigment epithelium. The murine mutation pink-eyed unstable (p(un)) spontaneously reverts to a wild-type allele by homologous recombination. In a retinal pigment epithelium cell this results in pigmentation, which can be observed in the adult eye. The clonal expansion of such cells during development has provided insight into the pattern of retinal pigment epithelium development. In contrast to previous results with Atm, p53 and Gadd45, p(un) reversion events in p21 deficient mice did not show any significant change. These results suggest that p21 does not play any role in maintaining overall genomic stability by regulating homologous recombination frequencies during development. However, the absence of p21 caused a distinct change in the positions of the reversion events within the retinal pigment epithelium. Those events that would normally arrest to produce single cell events continued to proliferate uncovering a cell cycle dysregulation phenotype. It is likely that p21 is involved in controlling the developmental pattern of the retinal pigment. We also found a C57BL/6J specific p21 dependent ocular defect in retinal folding, similar to those reported in the absence of p53.
    MeSH term(s) Animals ; Body Patterning/physiology ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA Damage/physiology ; Eye/cytology ; Eye/growth & development ; Eye Abnormalities/genetics ; Gene Expression Regulation, Developmental ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Pigment Epithelium of Eye/cytology ; Pigment Epithelium of Eye/embryology ; Pigment Epithelium of Eye/growth & development ; Recombination, Genetic ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Cdkn1a protein, mouse ; Cyclin-Dependent Kinase Inhibitor p21 ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2006-01-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2005.08.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5555: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Effect of Ku86 and DNA-PKcs deficiency on non-homologous end-joining and homologous recombination using a transient transfection assay.

    Secretan, M B / Scuric, Z / Oshima, J / Bishop, A J R / Howlett, N G / Yau, D / Schiestl, R H

    Mutation research

    2004  Volume 554, Issue 1-2, Page(s) 351–364

    Abstract: In mammalian cells, DNA double-strand breaks are repaired by non-homologous end-joining and homologous recombination, both pathways being essential for the maintenance of genome integrity. We determined the effect of mutations in Ku86 and DNA-PK on the ... ...

    Abstract In mammalian cells, DNA double-strand breaks are repaired by non-homologous end-joining and homologous recombination, both pathways being essential for the maintenance of genome integrity. We determined the effect of mutations in Ku86 and DNA-PK on the efficiency and the accuracy of double-strand break repair by non-homologous end-joining and homologous recombination in mammalian cells. We used an assay, based on the transient transfection of a linearized plasmid DNA, designed to simultaneously detect transfection and recombination markers. In agreement with previous results non-homologous end-joining was largely compromised in Ku86 deficient cells, and returned to normal in the Ku86-complemented isogenic cell line. In addition, analysis of DNA plasmids recovered from Ku86 mutant cells showed an increased use of microhomologies at the nonhomologous end joining junctions, and displayed a significantly higher frequency of DNA insertions compared to control cells. On the other hand, the DNA-PKcs deficient cell lines showed efficient double-strand break repair by both mechanisms.
    MeSH term(s) Animals ; Antigens, Nuclear/genetics ; Base Sequence ; CHO Cells ; Cricetinae ; DNA Primers ; DNA-Activated Protein Kinase ; DNA-Binding Proteins/genetics ; Ku Autoantigen ; Protein-Serine-Threonine Kinases/genetics ; Recombination, Genetic/genetics ; Transfection
    Chemical Substances Antigens, Nuclear ; DNA Primers ; DNA-Binding Proteins ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Ku Autoantigen (EC 4.2.99.-)
    Language English
    Publishing date 2004-10-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 206607-5
    ISSN 1873-135X ; 0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    ISSN (online) 1873-135X
    ISSN 0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    DOI 10.1016/j.mrfmmm.2004.05.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1316: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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