Applied pressure enables efficient isolated mitochondrial transfer and stable mitochondrial DNA (mtDNA) transplantation into a range of mtDNA-depleted cell types to restore respiration.

A genetic approach documents that mitochondrial DNA moves from donor cells to recipient mtDNA-depleted cells in whole mitochondria and that this restores mitochondrial respiration and the capacity of the cells to form tumours.

Isotope tracing, mathematical modeling, and single-cell ATP analysis reveal changes in blood cell metabolism under various conditions, showing stressed hematopoietic stem cells support hematopoiesis through glycolytic ATP production via PFKFB3.

Transferred mitochondria do not always regulate cell behavior by simply restoring mitochondrial function, but rather, transferred mitochondria are dysfunctional, initiating downstream signaling and proliferation in response to reactive oxygen species.

Histone acetyl-transferase Kat2a preserves leukemia stem cells through frequent transcriptional firing of metabolic and regulatory gene promoters and maintenance of a largely invariant self-renewal program.

Mitochondria serve as a reservoir for the sorting of an miRNA into P-bodies and from there into exosomes secreted from human cultured cells.

A new type of mRNAs-loaded CD133⁺ vesicles, named intercellsome, mediate cell-cell communications to compensate intracellular proliferative signal deficit, representing a previously unrecognized mechanism of cell proliferation under stress.

Oxygen levels at the time of T cell activation are major determinants of function, even when T cells are subsequently expanded in high levels of oxygen.

In its capacity to switch into a heritable, prionogenic form, a conserved RNA-modifying enzyme epigenetically alters fundamental growth, aging, and protein synthesis properties of eukaryotic cells.

Macropinocytosis of the signalling receptor LPAR1, by an actin and CYRI-B-dependent mechanism, impacts on progression and spread of pancreatic cancer in a mouse model.