Targeted disruption of the mouse ferrochelatase gene producing an exon 10 deletion

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An exon 10 deletion in the mouse ferrochelatase gene has a dominant-negative effect and causes mild protoporphyria.

Protoporphyria is generally inherited as an autosomal dominant disorder. The enzymatic defect of protoporphyria is a deficiency in ferrochelatase, which chelates iron and protoporphyrin IX to form heme. Patients with protoporphyria have decreased ferrochelatase activities that range from 5% to 30% of normal caused by heterogeneous mutations in the ferrochelatase gene. The molecular mechanism by...

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RED CELLS An exon 10 deletion in the mouse ferrochelatase gene has a dominant-negative effect and causes mild protoporphyria

Protoporphyria is generally inherited as an autosomal dominant disorder. The enzymatic defect of protoporphyria is a deficiency in ferrochelatase, which chelates iron and protoporphyrin IX to form heme. Patients with protoporphyria have decreased ferrochelatase activities that range from 5% to 30% of normal caused by heterogeneous mutations in the ferrochelatase gene. The molecular mechanism by...

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Targeted disruption of Hoxd-10 affects mouse hindlimb development.

Targeted disruption of the Hoxd-10 gene, a 5' member of the mouse HoxD linkage group, produces mice with hindlimb-specific defects in gait and adduction. To determine the underlying causes of this locomotor defect, mutant mice were examined for skeletal, muscular and neural abnormalities. Mutant mice exhibit alterations in the vertebral column and in the bones of the hindlimb. Sacral vertebrae ...

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ژورنال

عنوان ژورنال: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

سال: 1999

ISSN: 0925-4439

DOI: 10.1016/s0925-4439(98)00096-9