Wenping Li

TL;DR: Reincorporation of in vitro transcribed/translated PBR, but not PBR missing the cholesterol-binding domain, into MA-10 mitochondria rescued the ability of the mitochondria to form steroids and the ability to respond to StAR and Tom/StAR proteins.

TL;DR: Results demonstrate that in utero DEHP exposure exerts both short-term and long-lasting effects on testicular steroidogenesis that might involve distinct molecular targets in fetal and adult Leydig cells.

TL;DR: It is proposed that PBR overexpression could serve as a novel prognostic indicator of an aggressive phenotype in breast, colorectal and prostate cancers, where elevated PBR expression is associated with tumor progression.

TL;DR: It is suggested that in fibroblasts and fibrosarcoma cells PBR drug ligands inhibit cell proliferation in a PBR-independent manner, and this results are in contrast to data reported on cells of epithelial origin, suggesting that the origin of the cells is crucial in defining the role of PBR in their proliferation.

TL;DR: The molecular and cellular mechanisms underlying the effects of MEHP on basal and human chorionic gonadotropin (hCG)-stimulated steroid production by MA-10 Leydig cells are addressed using a systems biology approach.