Search results for CYP17A1

Showing 16 results out of 18

×

Species

Types

Compartments

Reaction types

Search properties

Species

Types

Compartments

Reaction types

Search properties

Protein (7 results from a total of 9)

Identifier: R-HSA-193119
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601860
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601794
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601826
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601756
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601823
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093
Identifier: R-HSA-5601769
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: CYP17A1: P05093

Set (1 results from a total of 1)

Identifier: R-HSA-5601806
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane

Reaction (7 results from a total of 7)

Identifier: R-HSA-193068
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
Pregnenolone (PREG) and NADPH + H+ react to form 17alpha-hydroxypregnenolone (17aHPREG), NADP+, and H2O. Steroid 17 alpha hydroxylase/17,20 lyase (CYP17A1), associated with the endoplasmic reticulum membrane, catalyzes this reaction.
Identifier: R-HSA-193099
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
17Alpha-hydroxyprogesterone (17aHPROG), NADPH + H+, and O2 react to form 4-Androstene-3, 17-dione (ANDST), NADP+, H2O, and acetaldehyde. Steroid 17 alpha hydroxylase/17,20 lyase (CYP17A1), which also catalyzes 17-alpha-hydroxylation, catalyzes this lyase reaction.
Identifier: R-HSA-193070
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
17-alpha-hydroxypregnenolone, NADPH + H+, and O2 react to form DHA (dehydroepiandrostenedione), NADP+, H2O, and acetaldehyde. CYP17 (which also catalyzes 17-alpha-hydroxylation) catalyzes this lyase reaction. There are marked species differences in which substrate is used for this lyase activity. The human enzyme prefers 17alpha-pregnenolone (delta5 steroid) as substrate (Brock, BJ, Waterman, MR, 1999). Corticotropin (Adrenocorticotropic hormone, ACTH) acts through the ACTH receptor called melanocortin receptor type 2 (MC2R) to stimulate steroidogenesis, increasing the production of androgens (McKenna et al, 1997).
Identifier: R-HSA-193072
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
Progesterone (P4), NADPH + H+, and O2 react to form 17alpha-hydroxyprogesterone (17aHPROG), NADP+, and H2O. This reaction is catalyzed by steroid 17 alpha hydroxylase/17,20 lyase (CYP17A1), associated with the endoplasmic reticulum membrane.
Identifier: R-HSA-9035956
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
Steroid 17-alpha-hydroxylase/17,20 lyase (CYP17A1) mediates both 17-alpha-hydroxylase and 17,20-lyase activity, allowing the adrenal glands and gonads to synthesise both 17-alpha-hydroxylated glucocorticoids and sex steroids respectively (Kagimoto et al. 1998). Defects in CYP17A1 can cause Adrenal hyperplasia 5 (AH5), a form of congenital adrenal hyperplasia (CAH), a common recessive disease due to defective synthesis of cortisol and sex steroids. Mutations causing combined 17-alpha-hydroxylase/17,20-lyase deficiency include S106P, R96W, W17*, R362C, W406R and R96Q (Lin et al. 1991, Laflamme et al. 1996, Suzuki et al. 1998, Martin et al. 2003, Brooke et al. 2006). Mutations causing isolated 17,20-lyase deficiency are R358Q and R347H (Geller et al. 1997, Van den Akker et al. 2002).
Identifier: R-HSA-9035954
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
Steroid 17-alpha-hydroxylase/17,20 lyase (CYP17A1) mediates both 17-alpha-hydroxylase and 17,20-lyase activity, allowing the adrenal glands and gonads to synthesise both 17-alpha-hydroxylated glucocorticoids and sex steroids respectively (Kagimoto et al. 1998). Defects in CYP17A1 can cause Adrenal hyperplasia 5 (AH5), a form of congenital adrenal hyperplasia (CAH), a common recessive disease due to defective synthesis of cortisol and sex steroids. Mutations causing combined 17-alpha-hydroxylase/17,20-lyase deficiency include S106P, R96W, W17*, R362C, W406R and R96Q (Lin et al. 1991, Laflamme et al. 1996, Suzuki et al. 1998, Martin et al. 2003, Brooke et al. 2006). Mutations causing isolated 17,20-lyase deficiency are R358Q and R347H (Geller et al. 1997, Van den Akker et al. 2002).
Identifier: R-HSA-5601843
Species: Homo sapiens
Compartment: cytosol, endoplasmic reticulum membrane
Steroid 17-alpha-hydroxylase/17,20 lyase (CYP17A1) mediates both 17-alpha-hydroxylase and 17,20-lyase activity, allowing the adrenal glands and gonads to synthesise both 17-alpha-hydroxylated glucocorticoids and sex steroids respectively (Kagimoto et al. 1998). Defects in CYP17A1 can cause Adrenal hyperplasia 5 (AH5), a form of congenital adrenal hyperplasia (CAH), a common recessive disease due to defective synthesis of cortisol and sex steroids. Mutations causing combined 17-alpha-hydroxylase/17,20-lyase deficiency include S106P, R96W, W17*, R362C, W406R and R96Q (Lin et al. 1991, Laflamme et al. 1996, Suzuki et al. 1998, Martin et al. 2003, Brooke et al. 2006). Mutations causing isolated 17,20-lyase deficiency are R358Q and R347H (Geller et al. 1997, Van den Akker et al. 2002).

Pathway (1 results from a total of 1)

Identifier: R-HSA-5579028
Species: Homo sapiens
Steroid 17-alpha-hydroxylase/17,20 lyase (CYP17A1) mediates both 17-alpha-hydroxylase and 17,20-lyase activity, allowing the adrenal glands and gonads to synthesise both 17-alpha-hydroxylated glucocorticoids and sex steroids respectively (Kagimoto et al. 1998). Defects in CYP17A1 can cause Adrenal hyperplasia 5 (AH5), a form of congenital adrenal hyperplasia (CAH), a common recessive disease due to defective synthesis of cortisol and sex steroids. Common symptoms include mild hypocortisolism, ambiguous genitalia in genetic males or failure of the ovaries to function at puberty in genetic females, metabolic alkalosis due to hypokalemia and low-renin hypertension. CYP17A1 can have defects in either or both of 17-alpha-hydroxylase and 17,20-lyase activities thus patients can show combined partial 17-alpha-hydroxylase/17,20-lyase deficiency or isolated 17,20-lyase deficiency traits (Yanase et al. 1992, Kater & Biglieri 1994, Fluck & Miller 2006, Miller 2012).
Cite Us!