MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining. Hung et al.

Published: 11 July 2018| Version 1 | DOI: 10.17632/2wdg6wf9fx.1
Contributors:
Barry Sleckman,
Putzer Hung

Description

These are the original data files for the Molecular Cell manuscript titled "MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining" by Hung et al. The paper characterizes the role of a small disordered peptide MRI (modulator of retrovirus infection, also known as CYREN) in promoting non-homologous end joining (NHEJ). Specifically, MRI associates with diverse DNA damage response factors at its termini and increases their avidity for chromatin at DNA double-strand breaks (DSBs). Moreover, MRI functions redundantly with XLF in DSB repair, and the loss of both proteins severely impairs V(D)J recombination in lymphocytes and leads to embryonic lethality in mice. We thus purpose that MRI acts as an adaptor that helps to enhance the efficiency of NHEJ.

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