Alan D. D’Andrea

Sep 18, 2024 | nature.com | Miklos Diossy |Pranshu Sahgal |Judit Börcsök |Dávid Szüts |Alan D. D’Andrea |István Csabai | +2 more

AbstractWe analyzed genomic data from the prostate cancer of African- and European American men to identify differences contributing to racial disparity of outcome. We also performed FISH-based studies of Chromodomain helicase DNA-binding protein 1 (CHD1) loss on prostate cancer tissue microarrays. We created CHD1-deficient prostate cancer cell lines for genomic, drug sensitivity and functional homologous recombination (HR) activity analysis.

Sep 4, 2024 | nature.com | Xiao-feng Zheng |Aniruddha Guha Sarkar |Aleem Syed |Huy Nguyen |Bartłomiej Tomasik |Kaimeng Huang | +3 more

AbstractCDK1 has been known to be the sole cyclin-dependent kinase (CDK) partner of cyclin B1 to drive mitotic progression1. Here we demonstrate that CDK5 is active during mitosis and is necessary for maintaining mitotic fidelity. CDK5 is an atypical CDK owing to its high expression in post-mitotic neurons and activation by non-cyclin proteins p35 and p392.

Dec 11, 2023 | nature.com | Carter Grochala |Jennifer L. Guerriero |Gerburg Wulf |Brian Wolpin |Ben Z. Stanger |Andrew J. Aguirre | +1 more

Retraction to: Nature Communications https://doi.org/10.1038/s41467-023-37096-6, published online 13 March 2023RETRACTION NOTEThe Editors retracted this article because of concerns regarding a number of figures presented in this work. These concerns call into question the integrity of the data and the article’s overall scientific soundness.

Oct 19, 2023 | cell.com | Alan D. D’Andrea

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Sep 11, 2023 | nature.com | Michelle Swift |Rui Zhou |Aleem Syed |Panagiotis A. Konstantinopoulos |Alan D. D’Andrea |Yizhou Joseph He

AbstractThe extent and efficacy of DNA end resection at DNA double-strand breaks (DSB) determine the repair pathway choice. Here we describe how the 53BP1-associated protein DYNLL1 works in tandem with the Shieldin complex to protect DNA ends. DYNLL1 is recruited to DSBs by 53BP1, where it limits end resection by binding and disrupting the MRE11 dimer. The Shieldin complex is recruited to a fraction of 53BP1-positive DSBs hours after DYNLL1, predominantly in G1 cells.