Joshua R. Brickner

TL;DR: It is reported that BRCA proteins prevent nucleolytic degradation by protecting replication forks that have undergone fork reversal upon drug treatment, and a MUS81 and POLD3-dependent mechanism of rescue following the withdrawal of genotoxic agent.

TL;DR: A functional CRISPR screen for previously unknown regulators of cross-presentation was designed, and the BEACH domain–containing protein WDFY4 was identified as essential for cross- Presentation of cell-associated antigens by cDC1s in mice, but was not required for major histocompatibility complex class II presentation, nor forCross-Presentation by monocyte-derived dendritic cells.

TL;DR: Novel and exciting crosstalk mechanisms between ubiquitination and other post-translational modifications, many of which work synergistically with each other to activate signaling events and help recruit important DNA damage effector proteins, particularly BRCA1 and 53BP1.

TL;DR: A previously unrecognized ubiquitin-dependent pathway induced specifically to repair alkylation damage is revealed, shedding light on the molecular mechanism of X-linked trichothiodystrophy.

TL;DR: A novel, noncanonical mechanism by which an OTU family deubiquitinase regulates its substrates is revealed, and it is shown that loss of OTUD4, USP7, or USP9X in tumor cells makes them significantly more sensitive to alkylating agents.