Practice question

Sterols exhibit pleiotropy including biophysical modulation precursor provision signaling regulation but not direct ion conduction through pore formation or carrier mechanism. In plasma membrane cholesterol increases order parameter thickness decreases passive proton sodium permeability stabilizes liquid ordered rafts organizing receptors transporters signaling complexes cytoskeleton linkers. Metabolically cholesterol transported inner mitochondrial membrane StAR STAR D4 transfer cleaved CYP11A1 cytochrome P450 side chain cleavage to pregnenolone first step mineralocorticoids glucocorticoids androgens estrogens via hydroxysteroid dehydrogenases CYP17 CYP21 CYP11B2 CYP19 aromatase pathways producing aldosterone cortisol sex hormones. In plants stigmasterol sitosterol analogs similar structural support growth. Sterols regulate transcription via SCAP INSIG SREBP sensing ER cholesterol; low sterol releases SREBP Golgi proteolysis driving lipogenesis LDL receptor expression controlled feedback homeostasis. Ion transport itself executed ion channels NaV CaV K channels active pumps Na K ATPase Ca ATPase carriers SLC families whose activity modulated sterol environment lipid raft context localization but not performed by sterol molecules directly. Thus attributing ion transport intrinsic sterol function conflates regulator effector. Accurate distinction separates membrane biophysics endocrinology electrophysiology essential exam clarity and prevents misconceptions about sterol direct transport capability and channel formation incorrect conceptualization.