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Thomas Ried

Researcher at National Institutes of Health

Publications -  401
Citations -  34909

Thomas Ried is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Comparative genomic hybridization & Cancer. The author has an hindex of 90, co-authored 384 publications receiving 32851 citations. Previous affiliations of Thomas Ried include University of Göttingen & Heidelberg University.

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Multicolor Spectral Karyotyping of Human Chromosomes

TL;DR: Whole-genome scanning by spectral karyotyping allowed instantaneous visualization of defined emission spectra for each human chromosome after fluorescence in situ hybridization, and all human chromosomes were simultaneously identified.
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Atm-deficient mice: a paradigm of ataxia telangiectasia.

TL;DR: Atm-disrupted mice recapitulate the ataxia telangiectasia phenotype in humans, providing a mammalian model in which to study the pathophysiology of this pleiotropic disorder.
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SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin

TL;DR: The human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin and contributes to the propagation of a specialized chromatin state at mammalian telomeres, which in turn is required for proper telomere metabolism and function.
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Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells.

TL;DR: It is shown that mouse embryonic fibroblast cells carrying a targeted deletion of exon 11 of the Brca1 gene maintain an intact G1-S cell cycle checkpoint and proliferate poorly, however, a defective G2-M checkpoint in these cells is accompanied by extensive chromosomal abnormalities.
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Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice.

TL;DR: It is demonstrated that Sirt1(+/-) mice develop tumors in multiple tissues, whereas activation of SIRT1 by resveratrol treatment reduces tumorigenesis, and it is shown that many human cancers exhibit reduced levels ofSIRT1 compared to normal controls.