Steroid: Difference between revisions

Revision as of 16:20, 1 January 2008

Classification

Corticosteroids

(CC) Image: David E. Volk
Structures of cortisol, the major glucocorticoid, corticosterone and aldosterone, the major mineralcorticoid.

For more information, see: corticosteroids.

Glucocorticoids and mineralocorticoids (or mineralcorticoids) are naturally synthesized by the enzymatic oxidation of progesterone. Cortisol is produced when progesterone is hydroxylated at three positions, C-11, C-17 and C21. The oxidation of the C-17 carbon must occur before the hydroxylation at C-21 to synthesize cortisol, otherwise corticosterone is formed. Aldosterone, the major mineralcorticoid, is synthesized from corticosterone by oxidation of the C-18 methyl group to form an aldehyde.

Sex steroids

(CC) Image: David E. Volk
Add image caption here.

Androgens and estrogens have only nineteen or eighteen carbon atoms, respectively, compared to the larger progestagens, glucocorticoids and mineralcorticoids all have twenty one carbon atoms. The biosynthesis of both classes of sex steroids starts with the hydroxylation of progesterone at C-17 to produce 17 $\alpha$ -hydroxyprogesterone. Cleavage of the C20-C21 side chain and oxidation of the C-17 hydroxyl group into a ketone produces androstenedione. Reduction of the C-17 keto group of androstenedione yields testosterone, one of the most abused anabolic steroids. The smallest class of steroids, the estrogens, are biosynthesized from the androgens by loss of the C-19 $\beta$ -methyl group, reduction of the C-3 ketone to a hydroxyl group, and the formation of an aromatic ring A. Estradiol is the major estrogen.

Progestagens

Progesterone, vital to pregnancy.

Pregnenolone forms by removal of C22-C27 of cholesterol.

Pregnenolone is the first steroid derived from cholesterol. It is synthesized through an intermediate, 20 $\alpha$ ,22 $\beta$ -dihydroxy-cholesterol, which is subsequently oxidized at C-20 to form a ketone with cleavage of carbons 22-27.

Progesterone, a progestagen which prepares the lining of the uterus for implantation of an ovum, is biosynthesized from prognenolone by oxidation of the 3-hydroxy group into a 3-keto group and by the isomerization of the $\delta$ ⁵ double bond into a $\delta$ ⁴ double bond. This hormone is also essential to maintain pregnancy. Progresterone is the precursor chemical in the biosynthesis of corticoids and androgens.

Biochemistry

Synthesis

Cholesterol is the precursor from which all steroid hormones are synthesized. All steroid hormones have 21 or fewer carbons, although their precursor cholesterol has 27 carbon atoms. Because of this, all steroid numbering and nomenclature follow that of cholesterol. Some cholesterol derivatives have a proton added to the C-5 carbon. If the H-5 proton is $\alpha$ -oriented (points down) then rings A and B are fused in a trans conformation, but in the $\beta$ orientation, the rings are fused in a cis conformation. All steroids with an H5 are in the 5 $\alpha$ orientation, while bile salts derived from cholesterol have the opposite 5 $\beta$ orientation.

Mechanism of action

Steroids primary act by increasing gene expression and therefore must enter the nuclei of the target cells to upregulated gene express of specific proteins. Because of this mode of action, steroid hormones take hours to have an effect because messenger RNA and then proteins must be synthesized. This is in contrast with other fast acting hormones, such as epinephrine. The formation of the messenger RNA can be suppressed by actinomycin D. Steroids first bind tightly, with dissociation constants in the nanomolar range, to their receptor protein. This complex is tranlocated into the cell nucleus and binds to specific operator sites in the DNA. All steroid receptors have a DNA-bind region, often called the DNA-binding domain (or DBD), which is rich is the positively-charged amino acids arginine and lysine, and also contains many cysteines. The presence of a "Cys-X-X-Cys" motif (X=any amino acid) suggests the presence of a metal-binding finger. The receptors also have activatation factor domains at which additional cofactors must bind before the steroid:receptor complex can enter the nucleus or inititiate gene expression. Due to their complexity, hormone receptors are not well understood at this time and are the subject of intense research. However, no structures of steroid receptors in the unbound state have ever been determined to verify this. Several steroid:receptor complex structures have recently been determined. In addition to the DBD, all steroid hormone receptors have a hormone-binding region and the similarities in this region of the receptors suggests that they all had a common ancestor. The steroid receptor proteins are generally specific for each steroid class, binding tightly only to the target steroids, but weak binding can occur with other steroids for some of them. The thyroid-hormone receptor is similar in structure to the steroid receptors.

Medical uses of steroids

(CC) Image: David E. Volk
Prednisone is a cortisone mimic

Although cortisone can be used to treat inflammation related diseases, like rheumatoid arthritis, it has severe side effects. The drug prednisone and other glucocorticoids have been developed as a cortisone mimic and its use to leads to milder side effect problems in the patient population. The only difference between the two compounds is the presence of an double bond between the C1 and C2 carbons of prednisone (note arrows in figure). Cortisone has a single C-C bond in this location.

Diseases of steroid metabolism

Congenital Adrenal Hyperplasia

Congenital Adrenal Hyperplasia is "a group of inherited disorders of the adrenal glands, caused by enzyme defects in the synthesis of cortisol (hydrocortisone) and/or aldosterone leading to accumulation of precursors for androgens. depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. The most common defect is in steroid 21-hydroxylase. other defects occur in steroid 11-beta-hydroxylase; steroid 17-alpha-hydroxylase; or 3-beta-hydroxysteroid dehydrogenase ( 3-hydroxysteroid dehydrogenases)".^[1] ^[2]^[3]

Biochemistry

Some people inherit defective forms of the enzyme 21-hydroxylase. Because 21-hydroxylase is a key enzyme in the production of the corticosteroids, defects in this enzyme lead to severe physiological effects. The enzyme is required for the production of cortisol, corticosterone, aldosterone and other steroids. Diminished levels of the glucocorticoids induces the anteterior pituitary gland to increase production of ACTH, which in turn incrases the levels of progesterone and 17 $\alpha$ hydroxy-progesterone. High levels of these two hormones increases the levels of androgens, which are derived from them. The pathogenesis can be stopped by the administration of glucocorticoids to complete the feed-back mechanism and halt overproduction of ACTH.

Manifestations

Aldosterone is the main mineralcorticoid and is produced in the adrenal glands. It plays a critical role in retaining sodium ion concentrations and thus hydration, so patients with 21-hydroxylase deficiency can suffer hypertension and dehydration, which can lead to shock or death. Increases in the levels of the androgens (testosterone, for example) resulting from the overproduction of progesterone and 17 $\alpha$ hydroxy-progesterone lead to the virilization ((masculinization) of those affected. In females, masculinization of the external genitalia is usually evident at birth. Males appear normal at birth but sexual precocity soon follows. Accelerated growth and early bone development leads to a shortened stature.

References

↑ National Library of Medicine. Adrenal Hyperplasia, Congenital. Retrieved on 2008-01-01.
↑ Merke DP, Bornstein SR (2005). "Congenital adrenal hyperplasia". Lancet 365 (9477): 2125–36. DOI:10.1016/S0140-6736(05)66736-0. PMID 15964450. Research Blogging.
↑ Speiser PW, White PC (2003). "Congenital adrenal hyperplasia". N. Engl. J. Med. 349 (8): 776–88. DOI:10.1056/NEJMra021561. PMID 12930931. Research Blogging.

@@ Line 4: / Line 4: @@
 '''Steroids''', or '''steroid hormones''', are powerful hormones with drastic effects, both good and bad, when artificially supplimented into living systems.  They are normally produced by only three glands, the adrenal cortex, the testes, and the ovaries, but are also produced by the placenta during pregnancy.   They play a role in all stages of life from the embryo until death.  Corticosteroids, or synthetic mimics such as [[prednisone]], are used to treat inflamation related illnesses like asthma or rheumatoid arthritis, but they can have severe side effects.  Athletes have often taken anobolic steroids to improve muscle growth and athletic performance. Glucocorticoids play a role in metabolism and inflamation, and estrogens have been linked to cancer.  Testosterone and estrogen influence sexual traits (maleness/femaleness).  All steroid hormones are naturally synthesized from cholesterol (through pregnenolone) under the control of the [[anterior pituitary gland]], which produces [[andrenocorticotropic hormone]] (ACTH, or corticotropin), a polypeptide that stimulates the conversion of cholesterol to pregnenolone.  The five major classes of steroids are: [[progestagens]], [[glucocorticoids]], [[mineralcorticoids]], [[androgens]] and [[estrogens]].  The steroid hormones activate gene expression by binding to enhancer proteins, called [[steroid receptors]].  Deficiency of the enzyme [[21-hydroxylase]] is the most common steroid-related in-born metabolic disorder, but treatments are available for this condition.
+==Classification==
-== cholesterol ==
+===Corticosteroids===
-Cholesterol is the precursor from which all steroid hormones are synthesized.  Because of this, all steroid numbering and nomenclature follow that of cholesterol.  Some cholesterol derivatives have a proton added to the C-5 carbon.  If the H-5 proton is <math>\alpha</math>-oriented (points down) then rings A and B are fused in a ''trans'' conformation, but in the <math>\beta</math> orientation, the rings are fused in a ''cis'' conformation.  All steroids with an H5 are in the 5<math>\alpha</math> orientation, while [[bile salt|bile salts]] derived from cholesterol have the opposite 5<math>\beta</math> orientation.
+[[Image:Cortisol corticosterone aldosterone stickfig DEVolk.jpg|right|thumb|450px|{{#ifexist:Template:Cortisol corticosterone aldosterone stickfig DEVolk.jpg/credit|{{Cortisol corticosterone aldosterone stickfig DEVolk.jpg/credit}}<br/>|}}Structures of cortisol, the major glucocorticoid, corticosterone and aldosterone, the major mineralcorticoid.]]
+{{main|corticosteroids}}
+[[Glucocorticoid]]s and [[mineralocorticoid]]s (or mineralcorticoids) are naturally synthesized by the enzymatic oxidation of progesterone.  Cortisol is produced when progesterone is hydroxylated at three positions, C-11, C-17 and C21.  The oxidation of the C-17 carbon must occur before the hydroxylation at C-21 to synthesize cortisol, otherwise corticosterone is formed.  Aldosterone, the major mineralcorticoid, is synthesized from corticosterone by oxidation of the C-18 methyl group to form an aldehyde.
+===Sex steroids===
+[[Image:Androgen estrogen synthesis structures.jpg|right|thumb|400px|{{#ifexist:Template:Androgen estrogen synthesis structures.jpg/credit|{{Androgen estrogen synthesis structures.jpg/credit}}<br/>|}}Add image caption here.]]
+[[Androgens]] and [[estrogens]] have only nineteen or eighteen carbon atoms, respectively, compared to the larger progestagens, glucocorticoids and mineralcorticoids all have twenty one carbon atoms.  The biosynthesis of both classes of sex steroids starts with the hydroxylation of progesterone at C-17 to produce 17<math>\alpha</math>-hydroxyprogesterone.  Cleavage of the C20-C21 side chain and oxidation of the C-17 hydroxyl group into a ketone produces [[androstenedione]].  Reduction of the C-17 keto group of androstenedione yields [[testosterone]], one of the most abused [[anabolic steroids]].  The smallest class of steroids, the estrogens, are biosynthesized from the androgens by loss of the C-19 <math>\beta</math>-methyl group, reduction of the C-3 ketone to a hydroxyl group, and the formation of an aromatic ring A.  [[Estradiol]] is the major estrogen.
-== pregnenolone and [[progestagens]] ==
+===Progestagens===
 [[Image:Progesterone DEVolk.jpg|right|thumb|200px| Progesterone, vital to pregnancy.]]
 [[Image:Pregnenolone DEVolk.jpg|left|thumb|200px|Pregnenolone forms by removal of C22-C27 of cholesterol.]]
-All steroid hormones have 21 or fewer carbons, although their precursor chemical, cholesterol, has 27 carbon atoms.  '''Pregnenolone''' is the first steroid derived from cholesterol.  It is synthesized through an intermediate, 20<math>\alpha</math>,22<math>\beta</math>-dihydroxy-cholesterol, which is subsequently oxidized at C-20 to form a ketone with cleavage of carbons 22-27.
+'''Pregnenolone''' is the first steroid derived from cholesterol.  It is synthesized through an intermediate, 20<math>\alpha</math>,22<math>\beta</math>-dihydroxy-cholesterol, which is subsequently oxidized at C-20 to form a ketone with cleavage of carbons 22-27.
-Progesterone, a progestagen which prepares the lining of the uterus for implantation of an ovum, is biosynthesized from prognenolone by oxidation of the 3-hydroxy group into a 3-keto group and by the [[isomerization]] of the <math>\delta</math><sup>5</sup> double bond into a <math>\delta</math><sup>4</sup> double bond.  This hormone is also essential to maintain pregnancy.  Progresterone is the precursor chemical in the biosynthesis of corticoids and androgens.
+Progesterone, a [[progestagen]] which prepares the lining of the uterus for implantation of an ovum, is biosynthesized from prognenolone by oxidation of the 3-hydroxy group into a 3-keto group and by the [[isomerization]] of the <math>\delta</math><sup>5</sup> double bond into a <math>\delta</math><sup>4</sup> double bond.  This hormone is also essential to maintain pregnancy.  Progresterone is the precursor chemical in the biosynthesis of corticoids and androgens.
+==Biochemistry==
+===Synthesis===
+Cholesterol is the precursor from which all steroid hormones are synthesized.  All steroid hormones have 21 or fewer carbons, although their precursor cholesterol has 27 carbon atoms.  Because of this, all steroid numbering and nomenclature follow that of cholesterol.  Some cholesterol derivatives have a proton added to the C-5 carbon.  If the H-5 proton is <math>\alpha</math>-oriented (points down) then rings A and B are fused in a ''trans'' conformation, but in the <math>\beta</math> orientation, the rings are fused in a ''cis'' conformation.  All steroids with an H5 are in the 5<math>\alpha</math> orientation, while [[bile salt|bile salts]] derived from cholesterol have the opposite 5<math>\beta</math> orientation.
+===Mechanism of action===
+Steroids primary act by increasing gene expression and therefore must enter the nuclei of the target cells to upregulated gene express of specific proteins.  Because of this mode of action, steroid hormones take hours to have an effect because messenger RNA and then proteins must be synthesized.  This is in contrast with other fast acting hormones, such as [[epinephrine]].  The formation of the messenger RNA can be suppressed by [[actinomycin D]].  Steroids first bind tightly, with dissociation constants in the nanomolar range, to their receptor protein.  This complex is tranlocated into the cell nucleus and binds to specific operator sites in the DNA.  All steroid receptors have a DNA-bind region, often called the DNA-binding domain (or DBD), which is rich is the positively-charged amino acids arginine and lysine, and also contains many cysteines.  The presence of a "Cys-X-X-Cys" motif (X=any amino acid) suggests the presence of a metal-binding finger.  The receptors also have activatation factor domains at which additional cofactors must bind before the steroid:receptor complex can enter the nucleus or inititiate gene expression. Due to their complexity, hormone receptors are not well understood at this time and are the subject of intense research.  However, no structures of steroid receptors in the unbound state have ever been determined to verify this. Several steroid:receptor complex structures have recently been determined. In addition to the DBD, all steroid hormone receptors have a hormone-binding region and the similarities in this region of the receptors suggests that they all had a common ancestor.  The steroid receptor proteins are generally specific for each steroid class, binding tightly only to the target steroids, but weak binding can occur with other steroids for some of them.  The [[thyroid-hormone receptor]] is similar in structure to the steroid receptors.
+==Medical uses of steroids==
+[[Image:Cortisone Prednisone stickfig DEVolk.jpg|right|thumb|350px|{{#ifexist:Template:Cortisone Prednisone stickfig DEVolk.jpg/credit|{{Cortisone Prednisone stickfig DEVolk.jpg/credit}}<br/>|}}Prednisone is a cortisone mimic]]
+Although cortisone can be used to treat inflammation related diseases, like rheumatoid arthritis, it has severe side effects.  The drug prednisone and other [[glucocorticoid]]s have been developed as a cortisone mimic and its use to leads to milder side effect problems in the patient population.  The only difference between the two compounds is the presence of an double bond between the C1 and C2 carbons of prednisone (note arrows in figure).  Cortisone has a single C-C bond in this location.
-==Corticosteroids==
+==Diseases of steroid metabolism==
-[[Image:Cortisol corticosterone aldosterone stickfig DEVolk.jpg|right|thumb|450px|{{#ifexist:Template:Cortisol corticosterone aldosterone stickfig DEVolk.jpg/credit|{{Cortisol corticosterone aldosterone stickfig DEVolk.jpg/credit}}<br/>|}}Structures of cortisol, the major glucocorticoid, corticosterone and aldosterone, the major mineralcorticoid.]]
+===Congenital Adrenal Hyperplasia===
-{{main|corticosteroids}}
+Congenital Adrenal Hyperplasia is "a group of inherited disorders of the adrenal glands, caused by enzyme defects in the synthesis of cortisol (hydrocortisone) and/or aldosterone leading to accumulation of precursors for androgens. depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. The most common defect is in steroid 21-hydroxylase. other defects occur in steroid 11-beta-hydroxylase; steroid 17-alpha-hydroxylase; or 3-beta-hydroxysteroid dehydrogenase ( 3-hydroxysteroid dehydrogenases)".<ref name="title">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?term=Congenital+Adrenal+Hyperplasia |title=Adrenal Hyperplasia, Congenital |accessdate=2008-01-01 |author=National Library of Medicine |authorlink= |coauthors= |date= |format= |work= |publisher= |pages= |language= |archiveurl= |archivedate= |quote=}}</ref>
-[[Glucocorticoid]]s and [[mineralocorticoid]]s (or mineralcorticoids) are naturally synthesized by the enzymatic oxidation of progesterone.  Cortisol is produced when progesterone is hydroxylated at three positions, C-11, C-17 and C21.  The oxidation of the C-17 carbon must occur before the hydroxylation at C-21 to synthesize cortisol, otherwise corticosterone is formed.  Aldosterone, the major mineralcorticoid, is synthesized from corticosterone by oxidation of the C-18 methyl group to form an aldehyde.
+<ref name="pmid15964450">{{cite journal |author=Merke DP, Bornstein SR |title=Congenital adrenal hyperplasia |journal=Lancet |volume=365 |issue=9477 |pages=2125–36 |year=2005 |pmid=15964450 |doi=10.1016/S0140-6736(05)66736-0 |issn=}}</ref><ref name="pmid12930931">{{cite journal |author=Speiser PW, White PC |title=Congenital adrenal hyperplasia |journal=N. Engl. J. Med. |volume=349 |issue=8 |pages=776–88 |year=2003 |pmid=12930931 |doi=10.1056/NEJMra021561 |issn=}}</ref>
-== [[androgens]] and [[estrogens]]  ==
+;Biochemistry
-[[Image:Androgen estrogen synthesis structures.jpg|right|thumb|400px|{{#ifexist:Template:Androgen estrogen synthesis structures.jpg/credit|{{Androgen estrogen synthesis structures.jpg/credit}}<br/>|}}Add image caption here.]]
+Some people inherit defective forms of the enzyme 21-hydroxylase.  Because 21-hydroxylase is a key enzyme in the production of the corticosteroids, defects in this enzyme lead to severe physiological effects.  The enzyme is required for the production of cortisol, corticosterone, aldosterone and other steroids.  Diminished levels of the glucocorticoids induces the anteterior pituitary gland to increase production of ACTH, which in turn incrases the levels of progesterone and 17<math>\alpha</math>hydroxy-progesterone.  High levels of these two hormones increases the levels of androgens, which are derived from them. The pathogenesis can be stopped by the administration of glucocorticoids to complete the feed-back mechanism and halt overproduction of ACTH.
-While the progestagens, glucocorticoids and mineralcorticoids all have twenty one carbon atoms, the smaller androgens and estrogens have only nineteen or eighteen carbon atoms, respectively.  The biosynthesis of both classes of steroids starts with the hydroxylation of progesterone at C-17 to produce 17<math\alpha</math>-hydroxyprogesterone.  Cleavage of the C20-C21 side chain and oxidation of the C-17 hydroxyl group into a ketone produces [[androstenedione]].  Reduction of the C-17 keto group of androstenedione yields [[testosterone]], one of the most abused [[anabolic steroids]].  The smallest class of steroids, the estrogens, are biosynthesized from the androgens by loss of the C-19 <math>\beta</math>-methyl group, reduction of the C-3 ketone to a hydroxyl group, and the formation of an aromatic ring A.  Estradiol is the major estrogen.
-== 21-hydroxylase deficiency ==
+;Manifestations
-Some people inherit defective forms of the enzyme 21-hydroxylase.  Because 21-hydroxylase is a key enzyme in the production of the corticosteroids, defects in this enzyme lead to severe physiological effects.  The enzyme is required for the production of cortisol, corticosterone, aldosterone and other steroids.  Diminished levels of the glucocorticoids induces the anteterior pituitary gland to increase production of ACTH, which in turn incrases the levels of progesterone and 17<math>\alpha</math>hydroxy-progesterone.  High levels of these two hormones increases the levels of androgens, which are derived from them. The pathogenesis can be stopped by the administration of glucocorticoids to complete the feed-back mechanism and halt overproduction of ACTH.
+Aldosterone is the main mineralcorticoid and is produced in the adrenal glands.  It plays a critical role in retaining sodium ion concentrations and thus hydration, so patients with 21-hydroxylase deficiency can suffer hypertension and dehydration, which can lead to shock or death.  Increases in the levels of the androgens (testosterone, for example) resulting from the overproduction of progesterone and 17<math>\alpha</math>hydroxy-progesterone lead to the [[virilization]] ((masculinization) of those affected.  In females, masculinization of the external genitalia is usually evident at birth.  Males appear normal at birth but sexual precocity soon follows.  Accelerated growth and early bone development leads to a shortened stature.
-Aldosterone is the main mineralcorticoid and is produced in the adrenal glands.  It plays a critical role in retaining sodium ion concentrations and thus hydration, so patients with 21-hydroxylase deficiency can suffer hypertension and dehydration, which can lead to shock or death.  Increases in the levels of the androgens (testosterone, for example) resulting from the overproduction of progesterone and 17<math>\alpha</math>hydroxy-progesterone lead to the [[virilization]] ((masculinization) of those affected.  In females, masculinization of the external genitalia is usually evident at birth.  Males appear normal at birth but sexual precocity soon follows.  Accellerated growth and early bone development leads to a shortened stature.
+==References==
+<references/>
-== Cortisone and Prednisone ==
+==See also==
-[[Image:Cortisone Prednisone stickfig DEVolk.jpg|right|thumb|350px|{{#ifexist:Template:Cortisone Prednisone stickfig DEVolk.jpg/credit|{{Cortisone Prednisone stickfig DEVolk.jpg/credit}}<br/>|}}Prednisone is a cortisone mimic]]
+*[[Corticosteroid]]
-Although cortisone can be used to treat inflamation related diseases, like rheumatoid arthritis, it has severe side effects.  The drug prednisone was developed as a cortisone mimic and its use to leads to milder side effect problems in the patient population.  The only difference between the two compounds is the presence of an double bond between the C1 and C2 carbons of prednisone (note arrows in figure).  Cortisone has a single C-C bond in this location.
+**[[Glucocorticoid]]
-== hormone receptors and mechanism of action ==
+[[Category:CZ Live]] [[Category:Health Sciences Workgroup]]
-Steroids primary act by increasing gene expression and therefore must enter the nuclei of the target cells to upregulated gene express of specific proteins.  Because of this mode of action, steroid hormones take hours to have an effect because messenger RNA and then proteins must be synthesized.  This is in contrast with other fast acting hormones, such as [[epinephrine]].  The formation of the messenger RNA can be suppressed by [[actinomycin D]].  Steroids first bind tightly, with dissociation constants in the nanomolar range, to their receptor protein.  This complex is tranlocated into the cell nucleus and binds to specific operator sites in the DNA.  All steroid receptors have a DNA-bind region, often called the DNA-binding domain (or DBD), which is rich is the positively-charged amino acids arginine and lysine, and also contains many cysteines.  The presence of a "Cys-X-X-Cys" motif (X=any amino acid) suggests the presence of a metal-binding finger.  The receptors also have activatation factor domains at which additional cofactors must bind before the steroid:receptor complex can enter the nucleus or inititiate gene expression. Due to their complexity, hormone receptors are not well understood at this time and are the subject of intense research.  However, no structures of steroid receptors in the unbound state have ever been determined to verify this. Several steroid:receptor complex structures have recently been determined. In addition to the DBD, all steroid hormone receptors have a hormone-binding region and the similarities in this region of the receptors suggests that they all had a common ancestor.  The steroid receptor proteins are generally specific for each steroid class, binding tightly only to the target steroids, but weak binding can occur with other steroids for some of them.  The [[thyroid-hormone receptor]] is similar in structure to the steroid receptors.

Steroid: Difference between revisions

Revision as of 16:20, 1 January 2008

Contents

Classification

Corticosteroids

Sex steroids

Progestagens

Biochemistry

Synthesis

Mechanism of action

Medical uses of steroids

Diseases of steroid metabolism

Congenital Adrenal Hyperplasia

References

See also

Navigation menu

Steroid: Difference between revisions

Revision as of 16:20, 1 January 2008

Classification

Corticosteroids

Sex steroids

Progestagens

Biochemistry

Synthesis

Mechanism of action

Medical uses of steroids

Diseases of steroid metabolism

Congenital Adrenal Hyperplasia

References

See also

Navigation menu

Search