Mouse lacking heart-muscle adenine nucleotide translocator protein and methods
US6013858A · kind A · utility
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8Claims
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Key dates
| Filing date | Oct 31, 1997 |
| Grant date | Jan 11, 2000 |
| Priority date | — |
| Expiry date | Oct 31, 2017 |
Classification
- Technology area (CPC A)Human Necessities
- CPC primaryA01K2267/03
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
Provided are transgenic mice genetically engineered for a deficiency of the heart-skeletal muscle isoform of the adenine nucleotide translocator protein (Ant1). These mice exhibit histological, biochemical and physiological signs of deficiency in oxidative phosphorylation and energy generation, and these mice provide the first animal model for mitochondrial myopathy and hypertrophic cardiomyopathy. This animal model is used in methods for testing compounds for therapeutic value in treating failure to exchange ATP and ADP across the mitochondrial inner membrane, OXPHOS deficiency and in treating cardiac hypertrophy.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.