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PMID |
Sentence |
1 |
3386237
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Mitochondrial cytochrome P-450 concentrations were not affected by diabetes but steroid 11 beta-hydroxylase activity was greater in the diabetics than in controls after both 1 and 2 months.
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2 |
3386237
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Microsomal cytochrome P-450 concentrations were unaffected by diabetes but 21-hydroxylase activity was significantly lower in adrenal microsomes from diabetics than from controls.
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3 |
12803238
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Immunohistochemical staining for steroidogenic enzymes showed reactivity for P450sec, 3 beta-HSD, P450c17, P450c21 and P450c11.
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4 |
21536586
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Liver receptor homolog (LRH-1) is an orphan nuclear receptor (NR5A2) that regulates cholesterol homeostasis and cell plasticity in endodermal-derived tissues.
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5 |
21536586
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Expression levels of the cell cycle genes cyclin D1 and cyclin E1 as well as the antiapoptotic gene bcl-xl were unaltered in LRH-1 expressing islets.
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6 |
21536586
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In contrast, the steroidogenic enzymes CYP11A1 and CYP11B1 involved in glucocorticoid biosynthesis were both stimulated in transduced islets.
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7 |
21536586
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In parallel, graded overexpression of LRH-1 dose-dependently impaired glucose-induced insulin secretion.
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8 |
22654799
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We carried out immunohistochemistry for vascular endothelial growth factor (VEGF) and its receptor (VEGF-R2) in 157 ACC samples and nine normal adrenal glands.
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9 |
22654799
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VEGF and VEGF-R2 protein were expressed in 72 and 99% of ACC samples, respectively.
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10 |
22654799
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Sunitinib induced down-regulation of HSD3B2 mRNA and protein in ACC cell lines (mRNA: 1 μM 44 ± 16%*; 5 μM 22 ± 2%*; 10 μM 19 ± 4%*; protein: 1 μM 82 ± 8%; 5 μM 63 ± 8%*; 10 μM 55 ± 9%*).
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11 |
22654799
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CYP11B1 was down-regulated at mRNA but not at protein level and CYP11A1 remained unchanged.
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12 |
22654799
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Sunitinib exhibits anti-proliferative effects in vitro, and appears to specifically block adrenal steroidogenesis by down-regulation of HSD3B2, rendering it a promising option for treatment of ACC.
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13 |
23235923
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Control of CYP11B2/CYP11B1 expression ratio and consequences for the zonation of the adrenal cortex.
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14 |
23235923
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Access of corticotropin to glucocorticoid synthesis in adrenocortical cells is provided by the expression of the ACTH receptor (MC2R).
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15 |
23235923
|
Activation of the MC2R increases stimulatory G-protein, adenylyl cyclase, and protein kinase A (PKA) activities.
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16 |
23235923
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Sensitivity of adrenocortical cells to renin/angiotensin-2 is conferred by the expression of the inhibitory G-protein-linked angiotensin-2 type 1 receptor (AT1R) that additionally associates to the phospholipase C-activating G-protein q.
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17 |
23235923
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The AT1R is connected to the adrenal potassium sensory system and regulates calcium influx as well as phospholipase C-β (PLC-β) and thus calmodulin kinase-dependent transcription of steroidogenic enzymes.
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18 |
23235923
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While AT1R signaling suppresses the influence of corticotropin on the generation of cyclic adenosine monophosphate, the expression of the AT1R and its associated enzyme activities are under the control of glucocorticoids.
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