Vitamin D resistant rickets with alopecia: cultured skin fibroblasts exhibit defective cytoplasmic receptors and unresponsiveness to 1,25(OH)2D3.
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Ketoconazole blocks adrenal steroidogenesis by inhibiting cytochrome P450-dependent enzymesThe molecular basis of hereditary 1,25-dihydroxyvitamin D3 resistant rickets in seven related familiesThe role of nuclear hormone receptors in cutaneous wound repairGenetic Disorders of Vitamin D MetabolismA possible role of vitamin D receptors in regulating vitamin D activation in the kidney.An ochre mutation in the vitamin D receptor gene causes hereditary 1,25-dihydroxyvitamin D3-resistant rickets in three families1,25-Dihydroxyvitamin D3 production by human keratinocytes. Kinetics and regulation.Vitamin D-dependent rickets type II. Defective induction of 25-hydroxyvitamin D3-24-hydroxylase by 1,25-dihydroxyvitamin D3 in cultured skin fibroblasts.Vitamin D-endocrine system.Evidence for in vivo upregulation of the intestinal vitamin D receptor during dietary calcium restriction in the rat.Long-term nocturnal calcium infusions can cure rickets and promote normal mineralization in hereditary resistance to 1,25-dihydroxyvitamin D.Resistance to 1,25-dihydroxyvitamin D. Association with heterogeneous defects in cultured skin fibroblasts.Genetic defects of the 1,25-dihydroxyvitamin D3 receptor.Impaired stimulation of 25-hydroxyvitamin D-24-hydroxylase in fibroblasts from a patient with vitamin D-dependent rickets, type II. A form of receptor-positive resistance to 1,25-dihydroxyvitamin D3.Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant ricketsHereditary vitamin D resistant rickets caused by a novel mutation in the vitamin D receptor that results in decreased affinity for hormone and cellular hyporesponsiveness.Hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia resulting from a novel missense mutation in the DNA-binding domain of the vitamin D receptorCultured psoriatic fibroblasts from involved and uninvolved sites have a partial but not absolute resistance to the proliferation-inhibition activity of 1,25-dihydroxyvitamin D3.Vitamin D - Dependent Rickets, Type II Case Report.Vitamin D nutritional policy needs a vision for the future.The mechanism of end-organ resistance to 1 alpha,25-dihydroxycholecalciferol in the common marmoset.Cultured human keratinocytes cannot metabolize vitamin D3 to 25-hydroxyvitamin D3
P2860
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P2860
Vitamin D resistant rickets with alopecia: cultured skin fibroblasts exhibit defective cytoplasmic receptors and unresponsiveness to 1,25(OH)2D3.
description
1982 nî lūn-bûn
@nan
1982年の論文
@ja
1982年学术文章
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1982年学术文章
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1982年学术文章
@zh-hans
1982年学术文章
@zh-my
1982年学术文章
@zh-sg
1982年學術文章
@yue
1982年學術文章
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1982年學術文章
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name
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@en
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@nl
type
label
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@en
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@nl
prefLabel
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@en
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@nl
P2093
P356
P1476
Vitamin D resistant rickets wi ...... responsiveness to 1,25(OH)2D3.
@en
P2093
A Benderli
Z Hochberg
P304
P356
10.1210/JCEM-55-5-1020
P407
P577
1982-11-01T00:00:00Z