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Annalisa Masi

Researcher at Sapienza University of Rome

Publications -  45
Citations -  725

Annalisa Masi is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: DNA damage & Nucleotide excision repair. The author has an hindex of 14, co-authored 36 publications receiving 571 citations. Previous affiliations of Annalisa Masi include New York University.

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Fatty Acids in Membranes as Homeostatic, Metabolic and Nutritional Biomarkers: Recent Advancements in Analytics and Diagnostics

TL;DR: This review focuses on fatty acid biomarkers with two examples of recent lipidomic research and health applications: monounsaturated fatty acids and the analytical challenge offered by hexadecenoic fatty acids (C16:1); and the cohort of 10 fatty acids in phospholipids of red blood cell membranes and its connections to metabolic and nutritional status in healthy and diseased subjects.
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Structural basis for the recognition of diastereomeric 5′,8-cyclo-2′-deoxypurine lesions by the human nucleotide excision repair system

TL;DR: The locally impaired stacking interaction energies correlate with relative NER incision efficiencies, and explain these results on a structural basis in terms of differences in dynamic perturbations of the DNA backbone imposed by the R and S covalent 5′,8 bonds.
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Affinity of the anthracycline antitumor drugs Doxorubicin and Sabarubicin for human telomeric G-quadruplex structures

TL;DR: It is proved that Doxorubsicin and Sabarubicin bind to the human telomeric sequence, 5'-d[GGG(TTAGGG)(3)]-3' (21-mer), assuming a G-quadruplex structure in the presence of K(+).
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5',8-Cyclopurine Lesions in DNA Damage: Chemical, Analytical, Biological, and Diagnostic Significance.

TL;DR: This review describes the main recent achievements in the preparation of the cPu molecular library for analytical and DNA synthesis applications for the studies of the enzymatic recognition and repair mechanisms, their impact on transcription and genetic instability, and quantitative determination of the levels of lesions in various types of cells and animal model systems.
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A 5′, 8-cyclo-2′-deoxypurine lesion induces trinucleotide repeat deletion via a unique lesion bypass by DNA polymerase β

TL;DR: This study indicates that accumulation of cdPus in the human genome can lead to TNR instability via a unique lesion bypass by pol β.