Steroid deficiency syndromes in mice with targeted disruption of Cyp11a1

Meng Chun Hu, Nai Chi Hsu, Noomen Ben El Hadj, Chin I. Pai, Hsueh Ping Chu, Chi Kuang Leo Wang, Bon Chu Chung

研究成果: ジャーナルへの寄稿学術誌査読

118 被引用数 (Scopus)


Steroid deficiencies are diseases affecting salt levels, sugar levels, and sexual differentiation. To study steroid deficiency in more detail, we used a gene-targeting technique to insert a neo gene into the first exon to disrupt Cyp11a1, the first gene in steroid biosynthetic pathways. Cyp11a1 null mice do not synthesize steroids. They die shortly after birth, but can be rescued by steroid injection. Due to the lack of feedback inhibition by glucocorticoid, their circulating ACTH levels are exceedingly high; this results in ectopic Cyp21 gene expression in the testis. Male Cyp11a1 null mice are feminized with female external genitalia and underdeveloped male accessory sex organs. Their testis, epididymis, and vas deferens are present, but undersized. In addition, their adrenals and gonads accumulate excessive amounts of lipid. The lack of steroid production, abnormal gene expression, and aberrant reproductive organ development resemble various steroid deficiency syndromes, making these mice good models for studies of steroid function and regulation.

ジャーナルMolecular Endocrinology
出版ステータス出版済み - 2002

!!!All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 内分泌学


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