Background:The mechanism mediating hormone-induced steroidogenesis involves multiprotein complexes. Results: 14-3-3␥ is identified as a hormone-induced regulator of STAR function. Conclusion: 14-3-3␥ negatively regulates steroidogenesis by interacting with STAR, acting in a buffer capacity to sustain the STAR-mediated steroid formation for prolonged periods of time. Significance: Characterizing the mechanisms regulating steroidogenesis contributes to our understanding of how steroids are synthesized.
The principal site of regulation of steroid hormone biosynthesis is the transfer of cholesterol from the outer to inner mitochondrial membrane. Hormonal stimulation of steroidogenic cells promotes this mitochondrial lipid import through a multi-protein complex, termed the transduceosome, spanning the two membranes. The transduceosome complex is assembled from multiple proteins, such as the steroidogenic acute regulatory (STAR) protein and translocator protein (TSPO), and requires their targeting to the mitochondria for transduceosome function. The vast majority of mitochondrial proteins, including those participating in cholesterol import, are encoded in the nucleus. Their subsequent mitochondrial incorporation is performed through a series of protein import machineries located in the outer and inner mitochondrial membranes. Here we review our current knowledge of the mitochondrial cholesterol import machinery of the transduceosome. This is complemented with descriptions of mitochondrial protein import machineries and mechanisms by which these machineries assemble the transduceosome in steroidogenic mitochondria.
Employing this method a very satisfactory outcome was obtained while no ptosis was observed. Therefore, we recommend this safe technique for treating patients with a history of eyelid ptosis.
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