Engineered mesenchymal stem cells (MSCs) could produce mutant β-galactosidase and trigger nitric oxide (NO) release when the NO prodrug is systemically administered, which can achieve NO release in a precise spatiotemporal manner and augment the therapeutic efficiency of MSCs.

The molecular regulatory mechanisms that control the interaction between mesenchymal stem cells and transit amplifying cells to maintain tissue homeostasis.

Developing long bones contain distinct mesenchymal stem-cell populations derived from mesoderm and neural crest, which have specialized functions in skeleton formation and the establishment of the hematopoietic stem-cell niche, respectively.

The transcription factor C/EBPβ binds to different DNA sequences depending on whether it binds to ATF4, which enables C/EBPβ to conduct diverse transcriptional programs during adipocyte differentiation by exploiting an expanded motif repertoire.

The transcription factor PROP1 controls a genetic network that drives pituitary stem cells to undergo an epithelial-to-mesenchymal-like transition and differentiate.

The stanniocalcin-1-dependent immunosuppressive roles of mesenchymal stem cell on chimeric antigen receptor modified T cell therapy.

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.

Acute lymphoblastic and myeloblastic leukemias activate lymphotoxin beta receptor in mesenchymal stem cells in the bone marrow to turn off interleukin-7 production and lymphopoiesis and gain competitive advantage.

Age-stratified comparisons of gene expression in progeria patient fibroblasts reveals disruption of mesenchymal lineage pathways and points to a deficit in chondrogenic commitment in early development and a depletion of the mesenchymal lineage stem cell pool.

A key transcription-factor for osteogenic differentiation, PLZF, acts as a transcriptional activator by binding to active developmental enhancers and facilitates mediator recruitment, but is not involved in enhancer looping.