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Adam Cook

Researcher at University of Sydney

Publications -  22
Citations -  1112

Adam Cook is an academic researcher from University of Sydney. The author has contributed to research in topics: Chemistry & DNA repair. The author has an hindex of 10, co-authored 19 publications receiving 1012 citations. Previous affiliations of Adam Cook include Centre national de la recherche scientifique & Centenary Institute of Cancer Medicine and Cell Biology.

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Regulation of replication fork progression through histone supply and demand

TL;DR: It is proposed that Asf 1, as a histone acceptor and donor, handles parental and new histones at the replication fork via an Asf1–(H3-H4)–MCM2–7 intermediate and thus provides a means to fine-tune replication fork progression and histone supply and demand.
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HP1α recruitment to DNA damage by p150CAF-1 promotes homologous recombination repair

TL;DR: p150CAF-1-mediated recruitment of HP1α to DNA is essential for efficient assembly of DNA damage response complexes and subsequent homologous recombination repair.
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A Specific Function for the Histone Chaperone NASP to Fine-Tune a Reservoir of Soluble H3-H4 in the Histone Supply Chain

TL;DR: The data suggest that NASP does so by balancing the activity of the heat shock proteins Hsc70 and Hsp90 to direct H3-H4 for degradation by chaperone-mediated autophagy, and the existence of a tunable reservoir in mammalian cells demonstrates that contingency is integrated into the histone supply chain to respond to unexpected changes in demand.
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The HP1–p150/CAF-1 interaction is required for pericentric heterochromatin replication and S-phase progression in mouse cells

TL;DR: It is shown that p150, a subunit of chromatin assembly factor 1, has a key role in the replication of pericentric heterochromatin and S-phase progression in mouse cells, independently of its known function in histone deposition.
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Reduced Switching in SCID B Cells Is Associated with Altered Somatic Mutation of Recombined S Regions

TL;DR: It is shown that switching to all isotypes examined was detectable when the SCID mutation was introduced into anti-hen egg lysozyme transgenic B cells capable of undergoing class switch recombination, but switching was significantly reduced in comparison with control B cells of the same specificity lacking the RAG1 gene.