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Skd3 (human ClpB) is a potent ATP-dependent mitochondrial protein disaggregase that is activated by the rhomboid protease, PARL, and inactivated by MGCA7-linked mutations.

Phylogenomics provides support for the Gram-positive type of bacterial cell envelope being a derived character that arose independently multiple times through loss of an ancestral outer membrane.

HDAC3 regulates the development of pDCs and maintenance of homeostasis of hematopoietic progenitors with dendritic cell (DC) differentiation potential, mechanistically by repressing cDC1 associated genes in a deacetylase-dependent manner.

Caspase-11 catalytic activity and autoprocessing play key roles upstream rather than downstream of its assembly into higher-order inflammasome complexes in response to cytosolic bacterial lipopolysaccharide.

The AAA+ protein unfolding motor ClpX grips substrates with the uppermost part of its substrate-binding pore, and requires interactions with hydrophobic amino acid side chains to operate with optimal efficiency.

Single-cell RNA-seq data and transgenic models revealed B-plasmacytoid dendritic cells (B-pDCs) represent a phenotypically and functionally distinct common lymphoid progenitor-derived pDC lineage specialized in T cell activation and previously not described in mice.

TRIP13 inactivates the spindle assembly checkpoint by converting MAD2 from its active ‘closed’ state to its inactive ‘open’ state.

Single-cell RNA sequencing reveals HLJ1 as a novel immunomodulator for multicellular pathway of macrophages and NK cells, contributing to organ injury and sepsis death through amplified IL-12/IFN-γ axis.

Understanding of bacterial protein degradation is illuminated by cryo-EM structures of the substrate-bound ClpXP complex from Neisseria meningitidis at 2.3 to 3.3 Å resolution.

High resolution structures of the essential human AAA+ ATPase TorsinA and its disease mutant in complex with an activator reveal details of the interaction that will guide drug design and further functional characterization.