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Cartilage and bone tumors arise from chondrocyte or osteoblast progenitors but not differentiated cells or multipotent mesenchymal stem cells (MSCs) via the IHH-Wnt/β-Catenin pathway.

Perivascular extracellular vesicles induce bone repair, and do so via tetraspanin binding to recipient skeletal progenitor cells.

ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.

Myosin isoforms exhibit different functions in the formation of adherens junctions and the transmission of mechanical forces.

A mechanism for yeast centrosomes to differentiate the microtubule cytoskeleton.

Macrophages release 30-nm vesicular particles enriched in accessible cholesterol during cellular locomotion, a discovery that is likely relevant to cholesterol disposal by these cells.

In lateral roots, cells employ a novel pathway to cell edges to control directional growth, which acts independently of the leading paradigm of oriented deposition of cellulose microfibrils at faces.

Obesity leads to increased phosphatidylcholine turnover in adipose tissue macrophages that makes them susceptible to saturated fatty acid-induced inflammation.

The ER transmembrane protein VMP1 is important for release of lipoproteins from the ER membrane into the ER lumen for secretion.

Cells accumulate damaged proteins during aging and, by compromising the function of chaperones in folding newly synthesized G1 cyclins, proteostasis breakdown inhibits cell-cycle entry and drives yeast cells into senescence.