Another suggests that StAR acts in conjunction with PBR, causing the movement of Cl− out of the mitochondria to facilitate contact site formation.
[9] StAR has thus far been found in all tissues that can produce steroids, including the adrenal cortex, the gonads, the brain and the nonhuman placenta.
Substances that suppress StAR activity, like those listed below, can cause endocrine disrupting effects, including altered steroid hormone levels and fertility.
[10] Mutations that less severely affect the function of StAR result in nonclassic lipoid CAH or familial glucocorticoid deficiency type 3.
At the cellular level, the lack of StAR results in a pathologic accumulation of lipid within cells, especially noticeable in the adrenal cortex as seen in the mouse model.
It is important to note that no study has yet found a link between the loss of StAR and problems in bile acid production or increased risk for cardiovascular disease.
Recently StAR was found to be expressed in cardiac fibroblasts in response to ischemic injury due to myocardial infarction.
[22] The StAR protein was first identified, characterized and named by Douglas Stocco at Texas Tech University Health Sciences Center in 1994.
[23] The role of this protein in lipoid CAH was confirmed the following year in collaboration with Walter Miller at the University of California, San Francisco.
[24] All of this work follows the initial observations of the appearance of this protein and its phosphorylated form coincident with factors that caused steroid production by Nanette Orme-Johnson while at Tufts University.