Targeting the CRL5 ubiquitin ligase complex in combination with CDK9 or MCL1 inhibition could combat innate and acquired resistance of cancer cells to MCL1-targeting therapeutics.

Analysis of conformational heterogeneity in cryo-EM data by a recently developed deep learning method reveals the structure and dynamics of the oncogenic chromatin remodeler ALC1 bound to a poly-ADP-ribosylated nucleosome.

Neonatal ILC1-like cells are functionally immature but have the unique potential to generate NK cells characterized by downregulation of NKG2A and a highly diverse KIR receptor repertoire.

Analysis of a mouse model of megalencephalic leukoencephalopathy with subcortical cysts (MLC) shows that the astrocyte-specific membrane protein MLC1 sustains the postnatal development of perivascular astrocytic processes and that MLC is a developmental disorder of the gliovascular unit.

Retrograde signaling activates the Rad53 checkpoint kinase independently of the canonical DNA replication stress response.

DNA replication fork rate in budding yeast is regulated in response to DNA damage by phosphorylation of two proteins, Mrc1 and Mcm10, by the Rad53 protein kinase.

A technology to produce homogenously poly-ADP-ribosylated proteins reveals key molecular mechanisms that govern ATP-dependent chromatin remodeling activity at DNA damage sites.

Toxoplasma gondii infection leads to conversion of natural killer cells into cells resembling innate lymphoid cells, group 1, that circulate widely, disrupting current notions suggesting that these cells have distinct lineages.

MARCH5 mediates a pathway driving MCL1 degradation in response to cellular stress, which sensitizes to BH3 mimetic drugs targeting BCLXL and provides a broadly effective therapeutic strategy for solid tumors.

During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.