ライフサイエンスコーパス: steroid sulfatase

1 orneum function, beta-glucocerebrosidase and steroid sulfatase.

2 ncodes the steroid hormone-modulating enzyme steroid sulfatase.

3 sing for normal barrier homeostasis, neither steroid sulfatase activity nor mRNA levels are upregulat

4 The best non-steroidal inhibitor of steroid sulfatase activity was n-lauroyl tryamine phosph

5 were synthesized and tested as inhibitors of steroid sulfatase activity.

6 ctivity of the sulfamate derivatives against steroid sulfatase and carbonic anhydrase II (hCAII) was

7 2, E-cadherin, cyclooxygenase-2, aromatase, steroid sulfatase), and "proliferation factor" (cytokera

8 The neurobiological role of steroid sulfatase, and therefore its potential role in A

9 arrier homeostasis, and that basal levels of steroid sulfatase are sufficient to accommodate acute in

10 I), characterized by loss of function of the steroid sulfatase arylsulfatase C (STS), to develop a mo

11 With the acceptance of steroid sulfatase as a target for hormone-dependent canc

12 Steroid sulfatase catalyzes the hydrolysis of 3beta-hydr

13 nds into an aromatase homology model and the steroid sulfatase crystal structure are presented.

14 ull-length STS protein expression as well as steroid sulfatase enzymatic activity in proportion to th

15 In addition, the steroid sulfatase enzyme (STS) is putatively linked to f

16 Activities of beta-glucocerebrosidase and steroid sulfatase, enzymes previously linked to barrier

17 isome proliferator-activated receptor-gamma, steroid sulfatase, estrogen sulfonotransferase, and cyto

18 enhances brain cholinergic function and that steroid sulfatase inhibition may become an important too

19 Previous studies have demonstrated that the steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecan

20 Administration of the non-steroidal steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecan

21 treatment of these animals for 24 h with the steroid sulfatase inhibitor COUMATE at a dose (10 mg/kg,

22 ly change escape latency suggesting that the steroid sulfatase inhibitor did not alter motivation or

23 stat, as innovative dual-targeting aromatase-steroid sulfatase inhibitors (DASIs) and as multitargeti

24 rmone-dependent cancer, novel dual aromatase-steroid sulfatase inhibitors (DASIs) containing a sulfam

25 Steroid sulfatase inhibitors can alter the metabolism of

26 Steroid sulfatase inhibitors can enhance the concentrati

27 s suggest that the chronic administration of steroid sulfatase inhibitors enhance learning and spatia

28 results suggest that the arylsulfamate based steroid sulfatase inhibitors such as COUMATE interfere w

29 ulfamate (1) has been studied as a model for steroid sulfatase inhibitors such as Coumate, 667 Coumat

30 By introducting the steroid sulfatase inhibitory pharmacophore into aromatas

31 Hydrolysis of estrone 3-sulfate by steroid sulfatase is an important additional source of t

32 ynthetic enzymes beta-glucocerebrosidase and steroid sulfatase, markers of barrier maturation, were r

33 r epidermis and hydrolyzed to cholesterol by steroid sulfatase (SSase) in the SC.

34 Mutations in the gene for steroid sulfatase (SSase), are responsible for recessive

35 of CRI-S232-homologous repeats flanking the steroid sulfatase ( STS ) gene results in STS deletion,

36 A molecular candidate for this effect is Steroid sulfatase (Sts) as this is located in the pseudo

37 X-linked ichthyosis is the result of steroid sulfatase (STS) deficiency.

38 f the X-linked STS gene, encoding the enzyme steroid sulfatase (STS) influences risk for ADHD.

39 Migration was blocked by aromatase and steroid sulfatase (STS) inhibitors confirming intracrine

40 fatase inhibitors (DASIs), we introduced the steroid sulfatase (STS) inhibitory pharmacophore to letr

41 Steroid sulfatase (STS) is a new target for the endocrin

42 Estradiol-3,17-O,O-bis-sulfamates inhibit steroid sulfatase (STS), carbonic anhydrase (CA), and, w

43 The steroid sulfatase (STS)-mediated desulfation is a critic

44 ew potential hormone-dependent cancer target steroid sulfatase (STS).

45 treated by dual inhibition of aromatase and steroid sulfatase (STS).

46 h converts glucosylceramide to ceramide, and steroid sulfatase, which desulfates cholesterol sulfate,