ライフサイエンスコーパス: SRD5A2

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

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

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

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

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

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

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

8 1, SRD5A3, and AKR1C3, whereas expression of SRD5A2, CYP3A4, CYP3A5, and CYP3A7 was decreased.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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