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Georgios I. Karras

Researcher at Massachusetts Institute of Technology

Publications -  12
Citations -  2289

Georgios I. Karras is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: DNA repair & Eukaryotic DNA replication. The author has an hindex of 10, co-authored 10 publications receiving 2018 citations. Previous affiliations of Georgios I. Karras include Max Planck Society.

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Quantitative Analysis of Hsp90-Client Interactions Reveals Principles of Substrate Recognition

TL;DR: In this paper, the authors systematically and quantitatively surveyed most human kinases, transcription factors, and E3 ligases for interaction with HSP90 and its cochaperone CDC37.
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The macro domain is an ADP-ribose binding module

TL;DR: In this article, the authors provide biochemical and structural evidence that macro domains are high affinity binding modules for ADP-ribose nucleotide nucleotides and reveal a conserved ligand binding pocket among the macro domain fold.
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Widespread Macromolecular Interaction Perturbations in Human Genetic Disorders

TL;DR: This work functionally profile several thousand missense mutations across a spectrum of Mendelian disorders using various interaction assays, suggesting that disease-associated alleles that perturb distinct protein activities rather than grossly affecting folding and stability are relatively widespread.
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The RAD6 DNA damage tolerance pathway operates uncoupled from the replication fork and is functional beyond S phase

TL;DR: These findings indicate that both branches of the DNA damage tolerance pathway operate effectively after chromosomal replication, outside S phase, and propose that the RAD6 pathway acts on single-stranded gaps left behind newly restarted replication forks.
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HSP90 Shapes the Consequences of Human Genetic Variation

TL;DR: A compensatory FANCA somatic mutation from an "experiment of nature" in monozygotic twins both prevented anemia and reduced HSP90 binding and provides one plausible mechanism for the variable expressivity and environmental sensitivity of genetic diseases.