# |
PMID |
Sentence |
1 |
1174454
|
In addition to severe polydypsia, polyuria and polyphagia, these animals manifested super-normal glucose, triglycerides, free fatty acids and cholesterol in their blood, severe hepatic steatosis, adrenal hyperplasia with lipid depletion from the mineralocorticoid producing z. glomerulosa, thymus gland involution and complete degranulation of their insulin producing islet beta cells.
|
2 |
1828239
|
To test this hypothesis, we selected patients with polycystic ovary syndrome (PCO) and hypertestosteronemia and a group of individuals with adrenal hyperplasia (AH) and elevated DHEA and studied their 1) insulin and glucose responses to a 75-g oral glucose tolerance test, 2) insulin resistance by hypoglycemic responses to a standard dose of intravenous (IV) insulin, and 3) insulin binding and pyruvate dehydrogenase (PDH) responsiveness to insulin in phytohemagglutinin (PHA)-activated T lymphocytes.
|
3 |
2187189
|
Repopulation of the atrophied thymus in diabetic rats by insulin-like growth factor I.
|
4 |
2187189
|
We describe here that the weight and the architecture of the thymus of diabetic rats is restored towards normal not only by insulin but also by insulin-like growth factor I (IGF-I) treatment.
|
5 |
2187189
|
In contrast to insulin, this effect of IGF-I occurs despite persisting hyperglycemia and adrenal hyperplasia.
|
6 |
2187189
|
Insulin, as well as IGF-I treatment of diabetic rats increased [3H]thymidine incorporation by thymocytes.
|
7 |
2187189
|
In addition, a major deficiency of thymocytes expressing simultaneously the W3/25 and the Ox8 antigens (corresponding to immature human CD4+/CD8+ thymocytes) was observed.
|
8 |
2187189
|
These changes were restored towards normal by insulin as well as by IGF-I treatment.
|
9 |
2187189
|
We conclude that IGF-I has important effects on the thymocyte number and the presence of CD4+/CD8+ immature cells in the thymus of diabetic rats despite persisting hyperglycemia.
|
10 |
2537845
|
Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome.
|
11 |
2537845
|
Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome.
|
12 |
2537845
|
This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia.
|
13 |
2537845
|
Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.
|
14 |
2537845
|
Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome.
|
15 |
2537845
|
Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome.
|
16 |
2537845
|
This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia.
|
17 |
2537845
|
Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.
|
18 |
2537845
|
Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome.
|
19 |
2537845
|
Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome.
|
20 |
2537845
|
This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia.
|
21 |
2537845
|
Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.
|
22 |
2537845
|
Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome.
|
23 |
2537845
|
Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome.
|
24 |
2537845
|
This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia.
|
25 |
2537845
|
Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.
|
26 |
7916911
|
Steroidogenic enzymes P450scc, P450c17 and P450c21 have recently been shown to be the main autoantigens recognized by sera from patients with autoimmune polyglandular syndrome (APS type I) with or without Addison's disease.
|
27 |
7916911
|
We studied 50 patients with APS type I, 36 of whom also had Addison's disease, three patients with isolated (adult type) Addison's disease, seven healthy relatives of the patients with APS type I, 18 patients with insulin-dependent diabetes mellitus, 17 patients with autoimmune liver disease and 26 healthy controls.
|
28 |
7916911
|
The results thus indicate that P450scc and P450c17 enzymes are the precipitating adrenal autoantigens recognized by sera from APS type I patients.
|
29 |
7916911
|
Steroidogenic enzymes P450scc, P450c17 and P450c21 have recently been shown to be the main autoantigens recognized by sera from patients with autoimmune polyglandular syndrome (APS type I) with or without Addison's disease.
|
30 |
7916911
|
We studied 50 patients with APS type I, 36 of whom also had Addison's disease, three patients with isolated (adult type) Addison's disease, seven healthy relatives of the patients with APS type I, 18 patients with insulin-dependent diabetes mellitus, 17 patients with autoimmune liver disease and 26 healthy controls.
|
31 |
7916911
|
The results thus indicate that P450scc and P450c17 enzymes are the precipitating adrenal autoantigens recognized by sera from APS type I patients.
|
32 |
8773744
|
It is also possible that PCOS is truly polygenic and that CYP17 is one of several genes-including those related to insulin secretion and action-that contribute to the PCOS phenotype.
|
33 |
8817242
|
Whereas mitochondrial CYP11A (cytochrome P450cscc: cholesterol monooxygenase) was absolutely temperature-insensitive in all systems tested, CYP17 (cytochrome P450c17: steroid-17 alpha-monooxygenase/C17, 20-aldolase) in the smooth endoplasmic reticulum responded with a 57% loss in whole testes and 39% loss in purified Leydig cells upon a 3-hour temperature elevation from 31 degrees C to 38 degrees C.
|
34 |
8817242
|
It is concluded that CYP17, but not CYP11A, is very sensitive towards even moderate elevation of environmental temperature, and that this apparent lability is not an intrinsic property of the enzyme protein but rather mediated by heat-activated intracellular factors.
|
35 |
8817242
|
Whereas mitochondrial CYP11A (cytochrome P450cscc: cholesterol monooxygenase) was absolutely temperature-insensitive in all systems tested, CYP17 (cytochrome P450c17: steroid-17 alpha-monooxygenase/C17, 20-aldolase) in the smooth endoplasmic reticulum responded with a 57% loss in whole testes and 39% loss in purified Leydig cells upon a 3-hour temperature elevation from 31 degrees C to 38 degrees C.
|
36 |
8817242
|
It is concluded that CYP17, but not CYP11A, is very sensitive towards even moderate elevation of environmental temperature, and that this apparent lability is not an intrinsic property of the enzyme protein but rather mediated by heat-activated intracellular factors.
|
37 |
10754162
|
Adrenocorticotropic hormone-independent macronodular adrenal hyperplasia (AIMAH) was endocrinologically and histopathologically diagnosed.
|
38 |
10852471
|
The steroidogenic enzyme, 3beta-hydroxysteroid dehydrogenase (3betaHSD), has been characterized as a potential autoantigen in POF as well as in insulin-dependent diabetes mellitus (type 1 diabetes).
|
39 |
10852471
|
Here we studied the presence of steroid cell antibodies (SCA), autoantibodies to 3betaHSD and to two other known autoantigens in ovarian failure, steroidogenic enzymes 17alpha-hydroxylase (P450c17), and side-chain cleavage enzyme (P450scc) in POF patients and patient groups with autoimmune polyendocrinopathy syndromes type 1 and 2 (APS1 and -2), isolated Addison's disease, type 1 diabetes, and healthy controls.
|
40 |
10852471
|
The SCA were found in 2 of 48 POF, 11 of 15 APS1, and 1 of 9 APS2, and autoantibodies to in vitro translated 3betaHSD protein were detected in 1 POF serum associated with Addison's disease and 3 APS1 sera.
|
41 |
10852471
|
In analysis of autoantibodies to P450c17 and P450scc, antibodies to these enzymes were not found in POF sera, but were found in 10 and 12 APS1 patient sera, respectively, and 1 APS2 patient serum contained anti-P450c17 antibodies.
|
42 |
10852471
|
Our results show that autoantibodies to 3betaHSD in POF patients are rare and are also found in patients with APS1.
|
43 |
10852471
|
The steroidogenic enzyme, 3beta-hydroxysteroid dehydrogenase (3betaHSD), has been characterized as a potential autoantigen in POF as well as in insulin-dependent diabetes mellitus (type 1 diabetes).
|
44 |
10852471
|
Here we studied the presence of steroid cell antibodies (SCA), autoantibodies to 3betaHSD and to two other known autoantigens in ovarian failure, steroidogenic enzymes 17alpha-hydroxylase (P450c17), and side-chain cleavage enzyme (P450scc) in POF patients and patient groups with autoimmune polyendocrinopathy syndromes type 1 and 2 (APS1 and -2), isolated Addison's disease, type 1 diabetes, and healthy controls.
|
45 |
10852471
|
The SCA were found in 2 of 48 POF, 11 of 15 APS1, and 1 of 9 APS2, and autoantibodies to in vitro translated 3betaHSD protein were detected in 1 POF serum associated with Addison's disease and 3 APS1 sera.
|
46 |
10852471
|
In analysis of autoantibodies to P450c17 and P450scc, antibodies to these enzymes were not found in POF sera, but were found in 10 and 12 APS1 patient sera, respectively, and 1 APS2 patient serum contained anti-P450c17 antibodies.
|
47 |
10852471
|
Our results show that autoantibodies to 3betaHSD in POF patients are rare and are also found in patients with APS1.
|
48 |
10899497
|
Prevalence of 21-hydroxylase-deficient nonclassic adrenal hyperplasia and insulin resistance among hirsute women from Puerto Rico.
|
49 |
11170094
|
PE due to virilizing-type adrenal hyperplasia, caused by common mutations in the genes encoding for the adrenal enzymes 21-hydroxylase and 11-hydroxylase, was ruled out.
|
50 |
11572327
|
Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II.
|
51 |
11572327
|
With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests.
|
52 |
11572327
|
Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion.
|
53 |
11572327
|
An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable.
|
54 |
11572327
|
Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II.
|
55 |
11572327
|
With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests.
|
56 |
11572327
|
Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion.
|
57 |
11572327
|
An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable.
|
58 |
12044959
|
The mechanism of dissociation of cortisol and DHEA synthesis in aging depends on another regulator of 17,20-lyase of cytochrome P450c17 such as cytochrome P450 reductase.
|
59 |
12044959
|
We demonstrated significant decrease in cytochrome P450 reductase activity in bovine aged adrenal glands.
|
60 |
12044959
|
We clarified the conversion of DHEA to estrone by cytochrome P450 aromatase in primary cultured human osteoblasts.
|
61 |
12738163
|
The most common cause of androgen excess is the polycystic ovary syndrome (PCOS), with 21-hydroxylase-deficient nonclassic adrenal hyperplasia, the hyperandrogenic insulin-resistant acanthosis nigricans syndrome, androgen-secreting tumors, and androgenic drug intake occurring less frequently.
|
62 |
12803238
|
Immunohistochemical staining for steroidogenic enzymes showed reactivity for P450sec, 3 beta-HSD, P450c17, P450c21 and P450c11.
|
63 |
12887368
|
Adrenocorticotropin-independent macronodular adrenal hyperplasia treated by simultaneous bilateral laparoscopic adrenalectomy.
|
64 |
12887368
|
Radiological and endocrinological findings suggested adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
|
65 |
12887368
|
Adrenocorticotropin-independent macronodular adrenal hyperplasia treated by simultaneous bilateral laparoscopic adrenalectomy.
|
66 |
12887368
|
Radiological and endocrinological findings suggested adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
|
67 |
14709842
|
Unilateral adrenalectomy improves insulin resistance and diabetes mellitus in a patient with ACTH-independent macronodular adrenal hyperplasia.
|
68 |
15031776
|
Twelve women with polycystic ovary syndrome (PCOS), 10 women with idiopathic hirsutism (IH), and 10 women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) were studied.
|
69 |
15031776
|
The decrease in aMT6s excretion together with reduced serum LH, FSH, DHEAS and testosterone values during treatment with cyproterone acetate-ethinyl estradiol, suggest that sex steroids either directly or through the suppression of gonadotropins, modulate melatonin secretion in these patients.
|
70 |
15072549
|
Cinnamic acid based thiazolidinediones inhibit human P450c17 and 3beta-hydroxysteroid dehydrogenase and improve insulin sensitivity independent of PPARgamma agonist activity.
|
71 |
15072549
|
Thiazolidinediones improve insulin sensitivity in type 2 diabetes mellitus by acting as peroxisome proliferator-associated receptor gamma (PPARgamma) agonists, and decrease circulating androgen concentrations in polycystic ovary syndrome by unknown mechanisms.
|
72 |
15072549
|
Thus, the inhibition of P450c17 and 3betaHSDII by these novel thiazolidinediones reveals structure-activity relationships independent of PPARgamma transactivation.
|
73 |
15072549
|
Cinnamic acid based thiazolidinediones inhibit human P450c17 and 3beta-hydroxysteroid dehydrogenase and improve insulin sensitivity independent of PPARgamma agonist activity.
|
74 |
15072549
|
Thiazolidinediones improve insulin sensitivity in type 2 diabetes mellitus by acting as peroxisome proliferator-associated receptor gamma (PPARgamma) agonists, and decrease circulating androgen concentrations in polycystic ovary syndrome by unknown mechanisms.
|
75 |
15072549
|
Thus, the inhibition of P450c17 and 3betaHSDII by these novel thiazolidinediones reveals structure-activity relationships independent of PPARgamma transactivation.
|
76 |
16350721
|
Several genes from these pathways have been tested include genes involved in steroid hormone biosynthesis and metabolism (StAR, CYP11, CYP17, CYP19 HSD17B1-3, HSD3B1-2), gonadotropin and gonadal hormones action (ACTR1, ACTR2A-B, FS, INHA, INHBA-B, INHC, SHBG, LHCGR, FSHR, MADH4, AR), obesity and energy regulation (MC4R, OB, OBR, POMC, UCP2-3), insulin secretion and action (IGF1, IGF1R, IGFBPI1-3, INS VNTR, IR, INSL, IRS1-2, PPARG) and many others.
|
77 |
16350721
|
Polymorphic alleles of both IRS-1 and IRS-2 (insulin receptor substrate 1 - 2), alone or in combination, may have a functional impact on the insulin-resistant component of PCOS.
|
78 |
16350721
|
There is no evidence to suggest that follistatin gene polymorphisms play a role in the pathogenesis of insulin resistance in PCOS women.
|
79 |
16350721
|
The results of this study demonstrate that there are significant alterations in the expression of ERalpha and ERbeta in PCOS that may be related to abnormal follicular development.
|
80 |
16794802
|
Cushing's syndrome caused by adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is an extremely rare disease, which shows bilateral macronodular adrenal hypertrophy and autonomous cortisol production.
|
81 |
17218722
|
Familial adrenocorticotropin-independent macronodular adrenal hyperplasia with aberrant serotonin and vasopressin adrenal receptors.
|
82 |
17982690
|
The major genes in the up-regulated categories included Egr1, Saa2, Atf3, DNAJB1 and cCL2, whereas those in the down-regulated categories were Cyp17a1, Adn, Gadd45g, Eno3 and Moxd1.
|
83 |
18704836
|
On the other hand, E1S may be converted locally to free active estrogens via the action of steroid sulfatase (StS), which has been detected in specific parts of the bovine caruncular epithelium.
|
84 |
18704836
|
The down-regulation of P450scc and P450c17 and the up-regulation of 3beta-HSD and aromatase during the differentiation of TGC from UTC in parallel with the up-regulation of ER beta and estrogen sulfotransferase in maturing TGC suggests a function of placental estrogens primarily as autoor intracrine regulators during this process and assigns to conjugated placental estrogens a role as inactivated by-products of TGC differentiation intended for excretion.
|
85 |
19813002
|
Accordingly, the patient was diagnosed as having ACTH-independent macronodular adrenal hyperplasia (AIMAH) with subclinical Cushing's syndrome associated with the aberrant expression of β-adrenergic receptors.
|
86 |
21324829
|
Corticotropin-independent macronodular adrenal hyperplasia associated with insulinoma.
|
87 |
22101210
|
The activities of both cytochrome P450 17α-hydroxylase/17,20 lyase and cytochrome P450 21-hydroxylase were significantly inhibited in COS-1 cells.
|
88 |
22101210
|
Quantification of 11βOH-A4 showed this metabolite to be a major product of steroidogenesis in H295R cells and we confirm, for the first time, that this steroid metabolite is the product of the hydroxylation of A4 by human cytochrome P450 11β-hydroxylase.
|
89 |
22238371
|
Association study of CYP17 and HSD11B1 in polycystic ovary syndrome utilizing comprehensive gene coverage.
|
90 |
22238371
|
Cytochrome P450-C17 enzyme (CYP17) is an important component of the androgen synthesis pathway, a pathway that is dysfunctional in polycystic ovary syndrome (PCOS).
|
91 |
22238371
|
Both CYP17 and HSD11B1 genes have been previously studied for their possible relationship with PCOS, yielding inconsistent results.
|
92 |
22238371
|
Two-hundred and eighty-seven Caucasian PCOS women and 187 Caucasian controls were genotyped for single nucleotide polymorphisms (SNPs) that were specifically chosen to allow full coverage of CYP17 and HSD11B1, including four SNPs in CYP17 and eight SNPs in HSD11B1.
|
93 |
22238371
|
Association study of CYP17 and HSD11B1 in polycystic ovary syndrome utilizing comprehensive gene coverage.
|
94 |
22238371
|
Cytochrome P450-C17 enzyme (CYP17) is an important component of the androgen synthesis pathway, a pathway that is dysfunctional in polycystic ovary syndrome (PCOS).
|
95 |
22238371
|
Both CYP17 and HSD11B1 genes have been previously studied for their possible relationship with PCOS, yielding inconsistent results.
|
96 |
22238371
|
Two-hundred and eighty-seven Caucasian PCOS women and 187 Caucasian controls were genotyped for single nucleotide polymorphisms (SNPs) that were specifically chosen to allow full coverage of CYP17 and HSD11B1, including four SNPs in CYP17 and eight SNPs in HSD11B1.
|
97 |
22238371
|
Association study of CYP17 and HSD11B1 in polycystic ovary syndrome utilizing comprehensive gene coverage.
|
98 |
22238371
|
Cytochrome P450-C17 enzyme (CYP17) is an important component of the androgen synthesis pathway, a pathway that is dysfunctional in polycystic ovary syndrome (PCOS).
|
99 |
22238371
|
Both CYP17 and HSD11B1 genes have been previously studied for their possible relationship with PCOS, yielding inconsistent results.
|
100 |
22238371
|
Two-hundred and eighty-seven Caucasian PCOS women and 187 Caucasian controls were genotyped for single nucleotide polymorphisms (SNPs) that were specifically chosen to allow full coverage of CYP17 and HSD11B1, including four SNPs in CYP17 and eight SNPs in HSD11B1.
|
101 |
22238371
|
Association study of CYP17 and HSD11B1 in polycystic ovary syndrome utilizing comprehensive gene coverage.
|
102 |
22238371
|
Cytochrome P450-C17 enzyme (CYP17) is an important component of the androgen synthesis pathway, a pathway that is dysfunctional in polycystic ovary syndrome (PCOS).
|
103 |
22238371
|
Both CYP17 and HSD11B1 genes have been previously studied for their possible relationship with PCOS, yielding inconsistent results.
|
104 |
22238371
|
Two-hundred and eighty-seven Caucasian PCOS women and 187 Caucasian controls were genotyped for single nucleotide polymorphisms (SNPs) that were specifically chosen to allow full coverage of CYP17 and HSD11B1, including four SNPs in CYP17 and eight SNPs in HSD11B1.
|
105 |
22790131
|
Usefulness and limitations of unilateral adrenalectomy for ACTH-independent macronodular adrenal hyperplasia in a patient with poor glycemic control.
|
106 |
22790131
|
Adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a rare disease which causes Cushing's syndrome.
|
107 |
22790131
|
Usefulness and limitations of unilateral adrenalectomy for ACTH-independent macronodular adrenal hyperplasia in a patient with poor glycemic control.
|
108 |
22790131
|
Adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a rare disease which causes Cushing's syndrome.
|
109 |
22969879
|
Association between cytochrome P450 promoter polymorphisms and ischemic stroke.
|
110 |
22969879
|
The human cytochrome P450 (CYP) superfamily includes at least 57 genes that encode enzymes with diverse metabolic and biosynthetic functions.
|
111 |
22969879
|
This study was conducted in order to investigate the associations between polymorphisms in CYP superfamily genes (CYP11B2, CYP17A1, CYP2B6, CYP2C9, CYP2E1 and CYP7A1) and ischemic stroke (IS).
|
112 |
22969879
|
The rs1799998 SNP of CYP11B2 and rs3808607 of CYP7A1 were related to diabetes mellitus in IS (p<0.05).
|
113 |
22969879
|
CYP11B2, CYP2E1 and CYP7A1 SNPs were associated with IS in the population studied.
|
114 |
23133444
|
Out of the 52 SNPs analyzed, four SNPs including rs5326 (DRD1), rs1004467 (CYP17A1), rs2960306 (GRK4), and rs11191548 (near NT5C2) in diabetic subjects and rs1530440 (C10orf107) in prediabetic subjects showed a modest association with hypertension (P = 0.0265, 0.0020, 0.0066, 0.0078, and 0.0015, resp; all were insignificant after Bonferroni correction).
|
115 |
23425648
|
Adrenocorticotropic hormone independent macronodular adrenal hyperplasia due to aberrant receptor expression: is medical treatment always an option?
|
116 |
17138841
|
Pioglitazone inhibits androgen production in NCI-H295R cells by regulating gene expression of CYP17 and HSD3B2.
|
117 |
17138841
|
Pioglitazone but not rosiglitazone inhibited the expression of the CYP17 and HSD3B2 genes.
|
118 |
17138841
|
Likewise, pioglitazone repressed basal and 8-bromo-cAMP-stimulated activities of CYP17 and HSD3B2 promoter reporters in NCI-H295R cells.
|
119 |
17138841
|
Although peroxisome proliferator-activated receptor gamma (PPARgamma) is the nuclear receptor for TZDs, suppression of PPARgamma by small interfering RNA technique did not alter the inhibitory effect of pioglitazone on CYP17 and HSD3B2 expression, suggesting that the action of pioglitazone is independent of PPARgamma.
|
120 |
17138841
|
On the other hand, treatment of NCI-H295R cells with mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) enhanced promoter activity and expression of CYP17.
|
121 |
17138841
|
Pioglitazone inhibits androgen production in NCI-H295R cells by regulating gene expression of CYP17 and HSD3B2.
|
122 |
17138841
|
Pioglitazone but not rosiglitazone inhibited the expression of the CYP17 and HSD3B2 genes.
|
123 |
17138841
|
Likewise, pioglitazone repressed basal and 8-bromo-cAMP-stimulated activities of CYP17 and HSD3B2 promoter reporters in NCI-H295R cells.
|
124 |
17138841
|
Although peroxisome proliferator-activated receptor gamma (PPARgamma) is the nuclear receptor for TZDs, suppression of PPARgamma by small interfering RNA technique did not alter the inhibitory effect of pioglitazone on CYP17 and HSD3B2 expression, suggesting that the action of pioglitazone is independent of PPARgamma.
|
125 |
17138841
|
On the other hand, treatment of NCI-H295R cells with mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) enhanced promoter activity and expression of CYP17.
|
126 |
17138841
|
Pioglitazone inhibits androgen production in NCI-H295R cells by regulating gene expression of CYP17 and HSD3B2.
|
127 |
17138841
|
Pioglitazone but not rosiglitazone inhibited the expression of the CYP17 and HSD3B2 genes.
|
128 |
17138841
|
Likewise, pioglitazone repressed basal and 8-bromo-cAMP-stimulated activities of CYP17 and HSD3B2 promoter reporters in NCI-H295R cells.
|
129 |
17138841
|
Although peroxisome proliferator-activated receptor gamma (PPARgamma) is the nuclear receptor for TZDs, suppression of PPARgamma by small interfering RNA technique did not alter the inhibitory effect of pioglitazone on CYP17 and HSD3B2 expression, suggesting that the action of pioglitazone is independent of PPARgamma.
|
130 |
17138841
|
On the other hand, treatment of NCI-H295R cells with mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) enhanced promoter activity and expression of CYP17.
|
131 |
17138841
|
Pioglitazone inhibits androgen production in NCI-H295R cells by regulating gene expression of CYP17 and HSD3B2.
|
132 |
17138841
|
Pioglitazone but not rosiglitazone inhibited the expression of the CYP17 and HSD3B2 genes.
|
133 |
17138841
|
Likewise, pioglitazone repressed basal and 8-bromo-cAMP-stimulated activities of CYP17 and HSD3B2 promoter reporters in NCI-H295R cells.
|
134 |
17138841
|
Although peroxisome proliferator-activated receptor gamma (PPARgamma) is the nuclear receptor for TZDs, suppression of PPARgamma by small interfering RNA technique did not alter the inhibitory effect of pioglitazone on CYP17 and HSD3B2 expression, suggesting that the action of pioglitazone is independent of PPARgamma.
|
135 |
17138841
|
On the other hand, treatment of NCI-H295R cells with mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) enhanced promoter activity and expression of CYP17.
|
136 |
17138841
|
Pioglitazone inhibits androgen production in NCI-H295R cells by regulating gene expression of CYP17 and HSD3B2.
|
137 |
17138841
|
Pioglitazone but not rosiglitazone inhibited the expression of the CYP17 and HSD3B2 genes.
|
138 |
17138841
|
Likewise, pioglitazone repressed basal and 8-bromo-cAMP-stimulated activities of CYP17 and HSD3B2 promoter reporters in NCI-H295R cells.
|
139 |
17138841
|
Although peroxisome proliferator-activated receptor gamma (PPARgamma) is the nuclear receptor for TZDs, suppression of PPARgamma by small interfering RNA technique did not alter the inhibitory effect of pioglitazone on CYP17 and HSD3B2 expression, suggesting that the action of pioglitazone is independent of PPARgamma.
|
140 |
17138841
|
On the other hand, treatment of NCI-H295R cells with mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) enhanced promoter activity and expression of CYP17.
|