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drug target
the ratio of HSD17B1 to HSD17B2 is a good indicator of tamoxifen treatment benefit, as post-menopausal patients with tumors expressing a high HSD17B1/HSD17B2 protein ratio have less benefit from tamoxifen treatment
evolution
3,17beta-hydroxysteroid dehydrogenase is a member of the short-chain dehydrogenase/reductase (SDR) superfamily
evolution
enzyme AKR1C35 is a member of the aldoketo reductase (AKR) 1C subfamily in the AKR superfamily
evolution
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enzyme Tsol-17betaHSD belongs to the short-chain dehydrogenase/reductase (SDR) protein superfamily, it shares motifs and activity with the type 3 enzyme of some other species
evolution
the enzyme belongs to the AKR1C family
evolution
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all three proteins (Rdh11/12-like 1-3) include conserved signatures of the SDR family, such as cofactor binding (TGXXXGXG), the catalytic mechanism (YXXXK), and the structural integrity (NVG or NAG) patterns. Japanese eel Rdh11/12-like 1 clusters with piscine Rdh11 and Rdh12, but the cluster is formed outside that of mammalian Rdh11 and Rdh12. In contrast, Rdh11/12-like 2 and Rdh11/12-like 3 form a clade with putative European eel Rdh11s and Rdh12s outside that of mammalian and piscine Rdh11/Rdh12
evolution
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3,17beta-hydroxysteroid dehydrogenase is a member of the short-chain dehydrogenase/reductase (SDR) superfamily
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malfunction
AKR1C3 siRNA reduces androgen receptor signaling in VCaP cells. Small-molecule inhibitors inhibit both the enzymatic and coactivator functions of AKR1C3 resulting in androgen-dependent prostate cancer and CRPC regression
malfunction
compared to the wild-type Comamonas testosteroni, degradation ability of testosterone and cholesterol is almost lost, and degradation of estradiol is decreased in the 3,17beta-HSD knockout mutant. Degradation of testosterone and cholesterol is obviously increased in the 3,17beta-HSD overexpression mutant. The growths in the medium with testosterone, cholesterol or estradiol are impaired in 3,17beta-HSD knockout mutant
malfunction
mutation of Val54Ala, but not Cys310Phe, significantly impairs the 3beta-hydroxysteroid dehydrogenase enzyme activity, suggesting that Val54 plays a critical role in recognition of the steroidal substrate
malfunction
knockdown of 17beta-HSD1 gene, HSD17B1, modulates the transcript profile of the hormone-dependent breast cancer cell line T47D, T47D, with 105 genes regulated 1.5 fold or higher in estradiol-independent manner
malfunction
knockdown of 17beta-HSD1 gene, HSD17B1, modulates the transcript profile of the hormone-dependent breast cancer cell line T47D, with 105 genes regulated 1.5fold or higher in estradiol-independent manner. Genes that are primarily involved in the cell cycle progression, such as the cyclin A2 gene, CCNA2, are generally down-regulated whereas genes involved in apoptosis and cell death, including the pro-apoptotic gene XAF1, IFIH1 and FGF12, are upregulated by 17beta-HSD1 knockdown
malfunction
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compared to the wild-type Comamonas testosteroni, degradation ability of testosterone and cholesterol is almost lost, and degradation of estradiol is decreased in the 3,17beta-HSD knockout mutant. Degradation of testosterone and cholesterol is obviously increased in the 3,17beta-HSD overexpression mutant. The growths in the medium with testosterone, cholesterol or estradiol are impaired in 3,17beta-HSD knockout mutant
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metabolism
Comamonas testosteroni strain ATCC11996 is a gram-negative bacterium which can use steroids as carbon and energy source. 3,17beta-HSD is an enzyme which is involved in the complete oxidative degradation of the steroid skeleton, induced in the presence of these compounds in the culture medium
metabolism
the enzyme catalyzes the last step in the biosynthesis of the potent androgen testosterone (T), by stereoselectively reducing the C17 ketone of 4-androstene-3,17-dione (4-dione), with NADPH as cofactor
metabolism
the enzyme catalyzes the last step in the biosynthesis of the potent androgen testosterone (T), by stereoselectively reducing the C17 ketone of 4-androstene-3,17-dione (4-dione), with NADPH as cofactor
metabolism
HSD17B1 is controlled by estradiol, dihydrotestosterone, and miRNAs, as well as modulated by several breast cancer related genes
metabolism
the enzyme catalyses the last step in estrogen activation
metabolism
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the enzyme is important in all basic steroidogenic pathways
metabolism
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the enzyme catalyzes the last step in the biosynthesis of the potent androgen testosterone (T), by stereoselectively reducing the C17 ketone of 4-androstene-3,17-dione (4-dione), with NADPH as cofactor
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metabolism
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Comamonas testosteroni strain ATCC11996 is a gram-negative bacterium which can use steroids as carbon and energy source. 3,17beta-HSD is an enzyme which is involved in the complete oxidative degradation of the steroid skeleton, induced in the presence of these compounds in the culture medium
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physiological function
key enzyme in cardenolide biosynthesis
physiological function
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17beta-hydroxysteroid dehydrogenase type 3 catalyzes the last step in the biosynthesis of the potent androgen testosterone by stereoselectively reducing the C17 ketone of 4-androstene-3,17-dione (4-dione), with NADPH as cofactor
physiological function
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17beta-hydroxysteroid dehydrogenases (17beta-HSD) are key enzymes involved in the formation (reduction) and inactivation (oxidation) of sex steroids. Taenia solium cysticerci are able to synthesize sex steroid hormones in vitro when precursors are provided in the culture medium
physiological function
3,17beta-hydroxysteroid dehydrogenase is a key enzyme in steroid degradation
physiological function
castration-resistant prostate cancer may occur by several mechanisms including the upregulation of androgen receptor, coactivators, and steroidogenic enzymes, including aldo keto reductase 1C3 (AKR1C3). AKR1C3 converts weaker 17-keto androgenic precursors to more potent 17-hydroxy androgens and is consistently the major upregulated gene in castration-resistant prostate cancer, CRPC. AKR1C3 enhances androgen signaling and prostate cancer xenograft growth. AKR1C3 is a receptor- and tissue-selective pharmacologically targetable coactivator that promotes prostate cancer growth, AKR1C3-dependent R1881-induced androgen receptor transactivation in HEK-293 cells
physiological function
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conversion of testosterone to 4-dione detected in abdominal adipose tissue is caused by 17beta-HSD type 2 which is localized in the vasculature of the adipose compartment
physiological function
enzyme AKR1C35 oxidizes various xenobiotic alicyclic alcohols using NAD+
physiological function
17beta-HSD1 may be involved in oncogenesis by favoring antiapoptosis pathway in breast cancer cells
physiological function
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Japanese eel retinol dehydrogenases 11/12-like 1-3 (Rdh11/12-like 1-3, EC 1.1.1.300) are 17-oxosteroid reductases involved in sex steroid synthesis. Catalysis of the conversion of A4 to T and E1 to E2 is performed by recombinant Rdh11/12-like 1
physiological function
the enzyme 17beta-HSD1 may be involved in oncogenesis by favoring antiapoptosis pathway in breast cancer cells and correborates with its previously shown role in increasing breast cancer cell proliferation. The gene regulation occurring in steroid-deprived conditions shows that 17beta-HSD1 can modulate endogenous gene expression in steroid-independent manners
physiological function
the enzyme increases breast cancer cell proliferation via a dual effect on 17-beta-estradiol and 5alpha-dihydrotestosterone levels and impacts gene expression and protein profile of breast cancer cells cultured in 17-beta-estradiol-contained medium
physiological function
the enzyme is involved in estrogen-dependent diseases
physiological function
the expression of 17beta-hydroxysteroid dehydrogenase 1 and 2 alone and in combination predicts outcome of patients with breast cancer
physiological function
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3,17beta-hydroxysteroid dehydrogenase is a key enzyme in steroid degradation
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physiological function
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key enzyme in cardenolide biosynthesis
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additional information
PhaR is a repressor that controls 3,17beta-HSD expression, phaR knock-out mutants grow at higher rates and produce more protein in the presence of steroids as carbon source. PhaR also regulates other genes that relate to steroid degradation. Estradiol and cholesterol both cannot induce betahsd gene expression in both wild-type and mutant Comamonas testosteroni
additional information
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PhaR is a repressor that controls 3,17beta-HSD expression, phaR knock-out mutants grow at higher rates and produce more protein in the presence of steroids as carbon source. PhaR also regulates other genes that relate to steroid degradation. Estradiol and cholesterol both cannot induce betahsd gene expression in both wild-type and mutant Comamonas testosteroni
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