Steroid response element

Sex hormone-binding globulin (SHBG) is thought to mainly function as a transporter and reservoir for the estradiol and testosterone sex hormones. However it has also been demonstrated that SHBG can bind to a cell surface receptor (SHBG-R). The SHBG-R has not been completely characterized. A subset of steroids are able to bind to the SHBG/SHBG-R complex resulting in an activation of adenylyl cyclase and synthesis of the cAMP second messenger. [19] Hence the SHBG/SHBG-R complex appears to act as a transmembrane steroid receptor that is capable of transmitting signals to the interior of cells.

This is a rare complication that may occur if a small hole is made in the fibrous sac and does not close up after the needle puncture. These small holes are only made in less than 1% of epidural injections and usually heal on their own. The spinal fluid inside can leak out, and when severe, the brain loses the cushioning effect of the fluid, which causes a severe headache when you sit or stand. These types of headaches occur typically about 2-3 days after the procedure and are positional - they come on when you sit or stand and go away when you lie down. If you do develop a spinal headache, it is OK to treat yourself. As long as you do not feel ill and have no fever and the headache goes away when you lay down, you may treat yourself with 24 hours of bed rest with bathroom privileges while drinking plenty of fluids. This almost always works. If it does not, contact the radiologist who performed the procedure or your referring physician. A procedure (called an epidural blood patch) can be performed in the hospital that has a very high success rate in treating spinal headaches.  

In response to lowered levels of cholesterol, the supply is increased both by activating the expression of the gene encoding the low-density lipoprotein (LDL) receptor, which plays a central role in cellular uptake of cholesterol, and by activating the genes encoding various enzymes involved in the de novo biosynthesis of cholesterol, such as HMG-CoA reductase and HMG-CoA synthase. The genes encoding these proteins contain a sterol response element (SRE) that is able to bind two SRE-binding proteins (SREBP-1 and SREBP-2). These two proteins are synthesized as high-molecular-weight molecules that are bound to cellular membranes; hence, they cannot enter the nucleus and activate transcription by binding to the SRE. Following a decrease in cholesterol levels, SREBP-1 and SREBP-2 are cleaved proteolytically, so that a smaller active fragment of each is released from the membrane; it enters the nucleus, where it binds to the SRE and activates transcription (2, 3).

AB - Transcription of the chicken ovalbumin gene is induced both in vivo and in vitro by four classes of steroid hormones. Recent experiments identified a steroid-dependent regulatory element (SDRE) in the 5′-flanking region of the ovalbumin gene between -900 and -521. To characterize the regulatory properties of the SDRE more precisely, additional mutations were created in this region, and fusion genes prepared by linking the ovalbumin 5′-flanking region and promoter to the chloramphenicol acetyltransferase structural gene. When the ovalbumin-chloramphenicol acetyltransferase fusion genes were transfected into steroid-responsive primary oviduct cells, mutants lacking sequences between -900 and -732 were no longer responsive to estrogen, corticosterone, progesterone, or dihydrotestosterone. The SDRE did not confer steroid-dependent expression on the heterologous thymidine kinase promoter by itself but did in conjunction with the negative regulatory element identified between -350 and -100. This suggests that the two elements act as a single functional entity and that the SDRE is not behaving as a typical steroid response element. Gel shift analyses revealed that two SDRE-protein complexes were formed when nuclear protein extracts were derived from estrogen-treated chicken oviduct but that only one complex was formed with extracts from estrogen-withdrawn oviduct or from other tissues. Neither an estrogen response element oligomer nor a glucocorticoid/progesterone response element oligomer competed for either of the DNA·protein complexes. Partially purified progesterone receptor also did not bind to the SDRE. These data indicate that induction of the ovalbumin gene by steroid hormones requires complex interactions involving both the SDRE and the negative regulatory element.

AB - A fundamental dilemma of steroid hormone regulation is how specific transcription is attained in vivo when several receptors recognize the same DNA sequence in vitro. We have identified an enhancer of the mouse sex-limited protein (Slp) gene that is activated by androgens but not by glucocorticoids in transfection. Induction requires a consensus hormone response element (HRE) and multiple auxiliary elements within 120 base pairs. Androgen specificity relies on a dual function to augment androgen but prevent glucocorticoid action from a site that both receptors can bind. The nonreceptor factors are the dominant force in transcriptional specificity, although HRE sequence variations can affect the stringency and magnitude of hormonal response. The effect of HRE variations suggests that receptor position is altered relative to the other factors. Thus protein interactions that elicit specific gene regulation are established by the array of DNA elements in a complex enhancer and can be modulated by subtle sequence differences that may influence precise protein contacts.

Steroid response element

steroid response element

AB - Transcription of the chicken ovalbumin gene is induced both in vivo and in vitro by four classes of steroid hormones. Recent experiments identified a steroid-dependent regulatory element (SDRE) in the 5′-flanking region of the ovalbumin gene between -900 and -521. To characterize the regulatory properties of the SDRE more precisely, additional mutations were created in this region, and fusion genes prepared by linking the ovalbumin 5′-flanking region and promoter to the chloramphenicol acetyltransferase structural gene. When the ovalbumin-chloramphenicol acetyltransferase fusion genes were transfected into steroid-responsive primary oviduct cells, mutants lacking sequences between -900 and -732 were no longer responsive to estrogen, corticosterone, progesterone, or dihydrotestosterone. The SDRE did not confer steroid-dependent expression on the heterologous thymidine kinase promoter by itself but did in conjunction with the negative regulatory element identified between -350 and -100. This suggests that the two elements act as a single functional entity and that the SDRE is not behaving as a typical steroid response element. Gel shift analyses revealed that two SDRE-protein complexes were formed when nuclear protein extracts were derived from estrogen-treated chicken oviduct but that only one complex was formed with extracts from estrogen-withdrawn oviduct or from other tissues. Neither an estrogen response element oligomer nor a glucocorticoid/progesterone response element oligomer competed for either of the DNA·protein complexes. Partially purified progesterone receptor also did not bind to the SDRE. These data indicate that induction of the ovalbumin gene by steroid hormones requires complex interactions involving both the SDRE and the negative regulatory element.

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