ライフサイエンスコーパス: SRD5A2

1 of potential adverse drug effects (DPYD and SRD5A2).

2 A, c.548-44 T > G and c.278delG mutations in SRD5A2.

3 d genes: decreased ar (2-fold) and increased srd5a2 (2.6-fold).

4 ther common recessive carrier genes included SRD5A2 (5-alpha reductase deficiency) at a rate of about

5 The enzyme product of SRD5A2, 5alpha-reductase type II, is responsible for con

6 , there is little evidence of a role for the SRD5A2 A49T variant in prostate cancer risk.

7 derlying enzyme catalysis and inhibition for SRD5A2 and other eukaryotic integral membrane steroid re

8 nes (AKR1C1, AKR1C2, AKR1C3, CYP3A4, SRD5A1, SRD5A2, and PGR) influenced breast cancer risk.

9 ses the use of methylation and expression of SRD5A2 as a gene signature to tailor therapies for prost

10 Here, we report a crystal structure of human SRD5A2 at 2.8 angstrom, revealing a unique 7-TM structur

11 We also reconstructed this mutation in the SRD5A2 cDNA, and overexpressed the enzyme in mammalian t

12 1, SRD5A3, and AKR1C3, whereas expression of SRD5A2, CYP3A4, CYP3A5, and CYP3A7 was decreased.

13 The steroid 5-alpha reductase type II gene (SRD5A2) encodes the enzyme which converts testosterone (

14 alyzed a candidate gene for prostate cancer, SRD5A2, encoding prostatic steroid 5alpha-reductase type

15 The human SRD5A2 gene encodes the prostatic (or type II) steroid 5

16 Mutations in the SRD5A2 gene have been linked to 5alpha-reductase deficie

17 The A49T aminoacid substitution in the SRD5A2 gene increased the risk of clinically significant

18 The A49T variant of the SRD5A2 gene may be a significant contributor to the inci

19 Two polymorphisms in the SRD5a2 gene, V89L (rs523349) and A49T (rs9282858), have

20 tatic (or type II) steroid 5alpha-reductase (SRD5A2) gene, the product of which controls metabolic ac

21 orphism of the 5alpha-reductase type 2 gene (SRD5A2) gives rise to a substitution of leucine (leu) fo

22 ucleotide polymorphism, A49T (rs9282858), in SRD5A2 has been implicated in prostate cancer risk; howe

23 Finasteride and dutasteride, as SRD5A2 inhibitors, are widely used antiandrogen drugs fo

24 Steroid 5-alpha-reductase type 2 (SRD5a2) is a critical enzyme in androgen metabolism.

25 Human steroid 5alpha-reductase 2 (SRD5A2) is an integral membrane enzyme in steroid metabo

26 e prostate through increased activity of the SRD5A2 locus in prostate cancer progression, in a subset

27 such as SLCO1B1, ACADSB, TCF4, HCP5, MOCOS, SRD5A2, MCCC2, DCC, and PRKN while several other mutatio

28 We also characterized all of the SRD5A2 missense substitutions biochemically and pharmaco

29 We note that two out of the three recurrent SRD5A2 missense substitutions increased 5alpha-reductase

30 and UGT2B17 and down-regulated expression of SRD5A2 (P < 0.001 for all).

31 Dysregulation of GOLM1 (P = .037), SRD5A2 (P = .023), and MKi67 (P = .023) predicted clinic

32 d17b3, suggesting a compensatory increase in SRD5A2 to maintain androgen bioactivity during HSD17B3 d

33 Mapping disease-causing mutations of SRD5A2 to our structure suggests molecular mechanisms fo

34 ot support a moderate to large effect of the SRD5A2 V89L polymorphism on plasma AAG levels or CaP ris

35 ted with prostate cancer including, AR, PSA, SRD5A2, VDR and CYP isoforms.

36 eased DHT levels as expression of AKR1C2 and SRD5A2 was reduced in these tumors compared with their p

37 sticular expression of another SRD5A enzyme, Srd5a2, was markedly increased in the absence of Hsd17b3

38 androgen-regulated gene expression (srd5a1, srd5a2) when incorporated with the CON diet but greater

39 ents, we identified mutations in HSD17B3 and SRD5A2 which are both required for human sexual differen

40 d-5alpha-reductase isoenzyme-1 (SRD5A1) over SRD5A2, which is otherwise the dominant isoenzyme expres

41 an difference = 8.8%, P = 7.37 x 10(-6)) and SRD5A2 with 3 alpha-androstanediol-glucuronide (rs220853

42 onship of the A49T and V89L polymorphisms at SRD5A2 with clinical and pathological tumor characterist