Membrane-initiated steroid signaling (MISS): genomic steroid action starts at the plasma membrane

Rapid stress‐induced corticosterone rise in the hippocampus reverses serial memory retrieval pattern

“…Indeed, bound with BSA, steroid-BSA is a plasma membrane impermeable complex which spare neuronal membrane binding capacity (Caldwell et al, 1995;Zheng et al, 1996;Makara and Haller, 2001) and electrophysiological properties (Zheng et al, 1996;Karst et al, 2005;Tasker et al, 2006). The use of corticosterone-BSA to evaluate the rapid nongenomic effects of corticosterone on neural activity was as yet only evidenced in vitro (Liu and Chen, 1995;Lou and Chen, 1998;Takahashi et al, 2002;Daufeldt et al, 2003;Qiu et al, 1998Qiu et al, , 2003Karst et al, 2005).…”

The biological roles of extracellular and intracytoplasmic glucocorticoids in skeletal cells

“…Some of these nongenomic responses take place extremely quickly, often within seconds, without the steroid entering the cell interior and they are obviously independent of the nuclear receptor-connected transcription and translation machinery [45].…”

“…Several lines of evidences support the concept that a carriermediated uptake process for steroids is operational in plasma membranes of steroid-hormone target tissues [45][46][47][48][49][50][51]. For example, highly purified fractions of osmotically active plasma membrane vesicles are discovered in rat and human liver cells, which may be served for glucocorticoids uptake, and there is competition mechanism for entry to the vesicles between glucocorticoids and several non-glucocorticoids steroids [45][46][47][48].…”

“…For example, highly purified fractions of osmotically active plasma membrane vesicles are discovered in rat and human liver cells, which may be served for glucocorticoids uptake, and there is competition mechanism for entry to the vesicles between glucocorticoids and several non-glucocorticoids steroids [45][46][47][48].…”

Steroid binding sites in liver membranes: Interplay between glucocorticoids, sex steroids, and pituitary hormones

“…The first is a cortisol-binding protein composed at least in part of two polypeptides of 52-and 57-kDa [16]. The second is an active transmembrane transporter of corticosterone, termed "steroid hormone recognition and effector complex" (SHREC) [17], which mediates import of glucocorticoids into hepatocytes and seems to be involved in rapid signaling as well as genomic glucocorticoid actions. However, the different subcellular localization, together with the fact that plasma membrane-glucocorticoid binding proteins exhibit different binding characteristics when compared to LAGS makes it unlikely that these plasma membrane glucocorticoid binding proteins and LAGS are the same entity.…”