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Model Characteristics - Model:
Men1loxp
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| Model Descriptor |
Men1loxp
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| Official Nomenclature |
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| Genotype |
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| Species |
Mouse (Mus musculus)
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| Strain |
Not specified
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| Is This a Tool Strain? |
No
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Developmental Stage
(applies only to Zebrafish) |
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| Experimental Design |
To determine whether the tissue-specific deletion of the Men1 gene resulted in a parathyroid-specific phenotype, crosses were performed between PTH-Cre-positive mice and mice with the Men1 gene flanked by loxP sites. The progeny of these crosses were genotyped, and five groups of animals were identified and matched by age and gender.
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| Phenotype |
The inactivation of the MEN1 tumor suppressor gene in patients leads to a constellation of changes in endocrine tissues, including parathyroid neoplasia, pituitary adenomas, pancreatic neuroendocrine tumors, and carcinoids. To study the pathophysiological consequences of the deletion of the MEN1 gene, we set out to create a mouse model of hyperparathyroidism resulting from the deletion of the Men1 gene in parathyroid tissue. We introduced a Men1 gene flanked by loxP sites into the mouse germ line and then used a parathyroid cell-specific promoter to drive the expression of Cre recombinase, resulting in the deletion of the Men1 gene. Here, we show that loss of Men1 gene function in the parathyroid glands of mice results in histological changes consistent with parathyroid neoplasia as well as systemic hypercalcemia. This model provides a means for dissecting the molecular basis of this familial cancer syndrome and may allow for the development of new strategies to treat related forms of hypercalcemia.
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| Website for add. info |
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| Breeding Notes |
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| Sex Distribution of the Phenotype |
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| Submitted by |
Libutti, Steven
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| Principal Investigator / Lab |
Libutti, Steven
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| Comment |
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| Model Availability: This model is available from |
| Strain |
Distributor |
Stock number |
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 Comments (Please login to submit new comments) |
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