Výsledky vyhledávání - "Annette L. Medhurst"

Data from DNA-PKcs and PARP1 Bind to Unresected Stalled DNA Replication Forks Where They Recruit XRCC1 to Mediate Repair

Autor: Thomas Helleday, Katheryn Meek, Benedikt M. Kessler, Freddie C. Hamdy, Huahao Shen, Xinming Song, Joanna McGouran, Oliver Mortusewicz, Zhengqiang Bao, Jessica A. Neal, Annette L. Medhurst, Zhihui Chen, Songmin Ying

A series of critical pathways are responsible for the detection, signaling, and restart of replication forks that encounter blocks during S-phase progression. Small base lesions may obstruct replication fork progression and processing, but the link b

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::361d727bfa99010c57d5878fb42ab6d2
https://doi.org/10.1158/0008-5472.c.6508290.v1

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Supplementary Figures from DNA-PKcs and PARP1 Bind to Unresected Stalled DNA Replication Forks Where They Recruit XRCC1 to Mediate Repair

Supplementary Figures. Sup. Fig. 1: Recuirtment of XRCC1 to stalled DNA replication forks is prevented by CtIP. Sup. Fig. 2: CK2 actiivty is required for stabilization of XRCC1 protein and its recuirtment to stalled forks. Sup. Fig. 3: Interaction of

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::78bf44daa454108d34aa053e4f9bf6ae
https://doi.org/10.1158/0008-5472.22411761

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DNA-PKcs and PARP1 bind to unresected stalled DNA replication forks where they recruit XRCC1 to mediate repair

Autor: Joanna F. McGouran, Xinming Song, Zhengqiang Bao, Freddie C. Hamdy, Huahao Shen, Katheryn Meek, Annette L. Medhurst, Songmin Ying, Jessica A. Neal, Oliver Mortusewicz, Zhihui Chen, Benedikt M. Kessler, Thomas Helleday

Publikováno v: Europe PubMed Central

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::69b3ca85259eab8a50898020de5435ea
https://doi.org/10.1158/0008-5472.can-15-0608

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ATR and Rad17 collaborate in modulating Rad9 localisation at sites of DNA damage

Autor: Roland Kanaar, Nicholas D. Lakin, Veronique A. J. Smits, Annette L. Medhurst, Ildem Akerman, Daniël O. Warmerdam, Edward H. Verwayen

Publikováno v: Journal of Cell Science, 121(23), 3933-3940. Company of Biologists Ltd

The cell cycle checkpoint kinase Chk1 is phosphorylated and activated by ATR in response to DNA damage and is crucial for initiating the DNA damage response. A number of factors act in concert with ATR to facilitate Chk1 phosphorylation, including Ra

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbdac397ea2b3be589666ea826956d1d
https://doi.org/10.1242/jcs.033688

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FAAP100 is essential for activation of the Fanconi anemia-associated DNA damage response pathway

Autor: Zhijiang Yan, Detlev Schindler, Minoru Takata, Amom Ruhikanta Meetei, Maureen E. Hoatlin, Reinhard Kalb, Johan P. de Winter, Yutong Xue, Masamichi Ishiai, Kornelia Neveling, Weidong Wang, Annette L. Medhurst, Hans Joenje, Anneke B. Oostra, Abdullah Mahmood Ali, Chen Ling, Arleen D. Auerbach

Publikováno v: The EMBO Journal. 26:2104-2114

The Fanconi anemia (FA) core complex plays a central role in the DNA damage response network involving breast cancer susceptibility gene products, BRCA1 and BRCA2. The complex consists of eight FA proteins, including a ubiquitin ligase (FANCL) and a

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e5a42cd6da19ba007bcab22c51c57cb2
https://doi.org/10.1038/sj.emboj.7601666

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Evidence for subcomplexes in the Fanconi anemia pathway

Autor: Jurgen Steltenpool, Chantal Fontaine, Hans Joenje, Annette L. Medhurst, Weidong Wang, Johan P. de Winter, Miriam Ferrer, Martin A. Rooimans, Rik J. Scheper, El Houari Laghmani, Amom Ruhikanta Meetei, Jan de Groot

Publikováno v: Blood. 108:2072-2080

Fanconi anemia (FA) is a genomic instability disorder, clinically characterized by congenital abnormalities, progressive bone marrow failure, and predisposition to malignancy. Cells derived from patients with FA display a marked sensitivity to DNA cr

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e271f05f64006121dd28d78b52257a91
https://doi.org/10.1182/blood-2005-11-008151

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A cross-linker-sensitive myeloid leukemia cell line from a 2-year-old boy with severe Fanconi anemia and biallelicFANCD1/BRCA2 mutations

Autor: Tara Clancy, Jill Clayton-Smith, Osborn B. Eden, Trevor F. Carr, Michael R. Green, William D. Fergusson, Hans Joenje, Annette L. Medhurst, Quinten Waisfisz, Stefan Meyer, Johan P. de Winter, Andrew M. Will, Lisa M. Barber, Fei Chen, G. Malcolm Taylor, Anneke B. Oostra

Publikováno v: Genes, Chromosomes and Cancer. 42:404-415

Fanconi anemia (FA) is a rare autosomal recessive disorder characterized by congenital and developmental abnormalities, hypersensitivity to DNA cross-linking agents such as mitomycin C (MMC), and strong predisposition to acute myeloid leukemia (AML).

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::35146c67776fe64894f2efb611a097ca
https://doi.org/10.1002/gcc.20153

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Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways

Autor: Nigel J. Jones, Johan P. de Winter, Alan Ashworth, Christopher G. Mathew, James Hejna, Shobbir Hussain, Emily Witt, Annette L. Medhurst, James B. Wilson, Jean-Yves Masson, Robb E. Moses, Adelina A. Davies, Sahana Ananth, Stephen C. West

Publikováno v: Hussain, S, Wilson, JB, dr. Medhurst, A L, Hejna, J, Witt, E, Ananth, S, Davies, A, Masson, JY, Moses, R, West, SC, de Winter, J P & Ashworth, A 2004, ' Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways ', Human Molecular Genetics, vol. 13, pp. 1241-1248 . https://doi.org/10.1093/hmg/ddh135
Human Molecular Genetics, 13, 1241-1248. Oxford University Press

Fanconi anaemia (FA) is a chromosomal instability disorder characterized by cellular sensitivity to DNA interstrand crosslinking agents and a high risk of cancer. Six of the eight proteins encoded by the known FA genes form a nuclear complex which is

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::495ea3cd5943427f3170b2408c79baed
https://hdl.handle.net/1871/26053

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Yeast two-hybrid screens imply involvement of fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport

Autor: Annette L. Medhurst, Christopher G. Mathew, Maureen E. Hoatlin, Pia A. J. Huber, Yu Zhi, Sabine Herterich, Tanja Reuter, Hans J. Gross, Hans Joenje, Holger Hoehn, Quinten Waisfisz

Publikováno v: Experimental Cell Research, 289(2), 211-221. Academic Press Inc.
Reuter, TY, Medhurst, AL, Waisfisz, Q, Zhi, Y, Herterich, S, Hoehn, H, Gross, HJ, Joenje, H, Hoatlin, ME, Mathew, CG & Huber, PA 2003, ' Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport ', Experimental Cell Research, vol. 289, no. 2, pp. 211-221 . https://doi.org/10.1016/S0014-4827(03)00261-1

Mutations in one of at least eight different genes cause bone marrow failure, chromosome instability, and predisposition to cancer associated with the rare genetic syndrome Fanconi anemia (FA). The cloning of seven genes has provided the tools to stu

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::31e012f4d6140a38778f431e7bbb8cf2
https://doi.org/10.1016/s0014-4827(03)00261-1

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