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1 orneum function, beta-glucocerebrosidase and steroid sulfatase.
2 ncodes the steroid hormone-modulating enzyme steroid sulfatase.
3  target a catalytic formylglycine residue of steroid sulfatases, a residue that is also conserved in
4 sing for normal barrier homeostasis, neither steroid sulfatase activity nor mRNA levels are upregulat
5          The best non-steroidal inhibitor of steroid sulfatase activity was n-lauroyl tryamine phosph
6 were synthesized and tested as inhibitors of steroid sulfatase activity.
7 ctivity of the sulfamate derivatives against steroid sulfatase and carbonic anhydrase II (hCAII) was
8  2, E-cadherin, cyclooxygenase-2, aromatase, steroid sulfatase), and "proliferation factor" (cytokera
9                  The neurobiological role of steroid sulfatase, and therefore its potential role in A
10 arrier homeostasis, and that basal levels of steroid sulfatase are sufficient to accommodate acute in
11 I), characterized by loss of function of the steroid sulfatase arylsulfatase C (STS), to develop a mo
12                       With the acceptance of steroid sulfatase as a target for hormone-dependent canc
13                                              Steroid sulfatase catalyzes the hydrolysis of 3beta-hydr
14 nds into an aromatase homology model and the steroid sulfatase crystal structure are presented.
15 ull-length STS protein expression as well as steroid sulfatase enzymatic activity in proportion to th
16                             In addition, the steroid sulfatase enzyme (STS) is putatively linked to f
17    Activities of beta-glucocerebrosidase and steroid sulfatase, enzymes previously linked to barrier
18 isome proliferator-activated receptor-gamma, steroid sulfatase, estrogen sulfonotransferase, and cyto
19                  Deletions spanning the STS (steroid sulfatase) gene at Xp22.31 are associated with X
20 enhances brain cholinergic function and that steroid sulfatase inhibition may become an important too
21  Previous studies have demonstrated that the steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecan
22          Administration of the non-steroidal steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecan
23 treatment of these animals for 24 h with the steroid sulfatase inhibitor COUMATE at a dose (10 mg/kg,
24 ly change escape latency suggesting that the steroid sulfatase inhibitor did not alter motivation or
25 stat, as innovative dual-targeting aromatase-steroid sulfatase inhibitors (DASIs) and as multitargeti
26 rmone-dependent cancer, novel dual aromatase-steroid sulfatase inhibitors (DASIs) containing a sulfam
27                                              Steroid sulfatase inhibitors can alter the metabolism of
28                                              Steroid sulfatase inhibitors can enhance the concentrati
29 s suggest that the chronic administration of steroid sulfatase inhibitors enhance learning and spatia
30 results suggest that the arylsulfamate based steroid sulfatase inhibitors such as COUMATE interfere w
31 ulfamate (1) has been studied as a model for steroid sulfatase inhibitors such as Coumate, 667 Coumat
32                          By introducting the steroid sulfatase inhibitory pharmacophore into aromatas
33           Hydrolysis of estrone 3-sulfate by steroid sulfatase is an important additional source of t
34 ynthetic enzymes beta-glucocerebrosidase and steroid sulfatase, markers of barrier maturation, were r
35 ding for Bmx nonreceptor tyrosine kinase and steroid sulfatase, respectively) partially regulate the
36 r epidermis and hydrolyzed to cholesterol by steroid sulfatase (SSase) in the SC.
37                    Mutations in the gene for steroid sulfatase (SSase), are responsible for recessive
38  of CRI-S232-homologous repeats flanking the steroid sulfatase ( STS ) gene results in STS deletion,
39  A novel approach for the dual inhibition of steroid sulfatase (STS) and 17beta-hydroxysteroid dehydr
40                                              Steroid sulfatase (STS) and 17beta-hydroxysteroid dehydr
41     A molecular candidate for this effect is Steroid sulfatase (Sts) as this is located in the pseudo
42         X-linked ichthyosis is the result of steroid sulfatase (STS) deficiency.
43 f the X-linked STS gene, encoding the enzyme steroid sulfatase (STS) influences risk for ADHD.
44     ELINA is exemplified in the discovery of steroid sulfatase (STS) inhibiting lanostane triterpenes
45       Migration was blocked by aromatase and steroid sulfatase (STS) inhibitors confirming intracrine
46 ,3-triazol-4-yl)phenol derivatives as potent steroid sulfatase (STS) inhibitors for the treatment of
47 fatase inhibitors (DASIs), we introduced the steroid sulfatase (STS) inhibitory pharmacophore to letr
48                                              Steroid sulfatase (STS) is a key enzyme involved in the
49                                              Steroid sulfatase (STS) is a new target for the endocrin
50    Estradiol-3,17-O,O-bis-sulfamates inhibit steroid sulfatase (STS), carbonic anhydrase (CA), and, w
51                                          The steroid sulfatase (STS)-mediated desulfation is a critic
52  treated by dual inhibition of aromatase and steroid sulfatase (STS).
53 ew potential hormone-dependent cancer target steroid sulfatase (STS).
54 h converts glucosylceramide to ceramide, and steroid sulfatase, which desulfates cholesterol sulfate,