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J.H.J. Hoeijmakers

Researcher at Erasmus University Rotterdam

Publications -  20
Citations -  1472

J.H.J. Hoeijmakers is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: DNA repair & Xeroderma pigmentosum. The author has an hindex of 8, co-authored 20 publications receiving 1428 citations.

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Targeted disruption of the cell-cycle checkpoint gene ATR leads to early embryonic lethality in mice

TL;DR: Targeted inactivation of ATR in mice by disruption of the kinase domain leads to early embryonic lethality before embryonic day 8.5 (E8.5), supporting the idea that loss of both alleles of the ATR gene, even at the ES-cell level, is lethal.
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Inactivation of the HR6B Ubiquitin-Conjugating DNA Repair Enzyme in Mice Causes Male Sterility Associated with Chromatin Modification

TL;DR: The phenotype of the first animal mutant in the ubiquitin pathway is reported: inactivation of the hHR6B-homologous gene in mice causes male infertility, and this findings provide a parallel between yeast sporulation and mammalian spermatogenesis and strongly implicate h HR6-dependent ubiquitination in chromatin remodeling.
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Mouse Rad54 affects DNA conformation and DNA-damage-induced Rad51 foci formation

TL;DR: Results of a topological assay suggested that purified human Rad54 (hRad54) protein can unwind double-stranded DNA at the expense of ATP hydrolysis, which could promote the formation or stabilization of hRad51-mediated joint molecules.
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Evidence for a repair enzyme complex involving ERCC1 and complementing activities of ERCC4, ERCC11 and xeroderma pigmentosum group F.

TL;DR: Complementation analysis in vitro of rodent CGs is accomplished by pairwise mixing of mutant extracts, and results show that mutants from groups 2, 3, 5 and XP‐A can complement all other CGs tested, however, selective non‐complementation in vitro was observed in mutual mixtures of groups 1, 4, 11 andXP‐F, suggesting that the complementing activities involved somehow affect each other.
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Postmeiotic transcription of X and Y chromosomal genes during spermatogenesis in the mouse.

TL;DR: Differential postmeiotic expression of the Y chromosomal genes Ubely and Sry is shown, with highest mRNA levels in round spermatids and cytoplasmic fragments, respectively, which may have implications for the understanding of X chromosome inactivation during sperMatogenesis and paternal genome imprinting.