Combining electron microscopy and solution scattering demonstrated that properdin oligomers adopt extended rigid and well-defined conformations that are integral to the biological function of this complement regulator.

Tsc2 inactivation in mouse mesenchymal progenitors produced tumors with vascular anomalies reminiscent of human angiomyolipomas, and a gene expression signature in Tsc2-deficient tissues which included Lgals3, as a novel potential biomarker for TSC1/2 loss.

C-mannosylation supports native folding of thrombospondin type 1 repeats in the endoplasmic reticulum and stabilizes the folded proteins by modulating the dynamics of the tryptophan-arginine ladder.

The Tsr2 carrier protein connects the nuclear import machinery with the ribosome assembly pathway.

In Streptomyces, the nucleoid-associated protein Lsr2 functions as a xenogenic silencer of foreign genes, and as a metabolic gatekeeper, repressing expression of both cryptic and well-studied specialized metabolic biosynthetic clusters.

The sialylation of RANK⁺TLR2⁺ monocytes contributes to osteoclastogenesis and bone destruction in rheumatoid arthritis.

The Toll-like receptor 2-4 genetic modification goat improves effectively resistance against Staphylococcus aureus infection by enhancing autophagy level, and it provides a novel strategy for challenge of S. aureus-caused infections.

Novel post-translational modification of pattern recognition receptor TLR2 has consequences in bacterial infection and inflammatory signaling.

Recognition of SARS-CoV-2 spike protein by innate immune sensor TLR2 leads to the induction of inflammatory mediators and constitutes a mechanism for cytokine storm during COVID-19.

The pathogenic success of Mycobacterium tuberculosis relies in part on its ability to blunt a component of the TLR2-dependent immune response.