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Model Characteristics - Model:
Disruption of cyclin D1 nuclear export and proteolysis accelerates mammary carcinogenesis in MMTV-D1T286A mice
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| Model Descriptor |
Disruption of cyclin D1 nuclear export and proteolysis accelerates mammary carcinogenesis in MMTV-D1T286A mice
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| Official Nomenclature |
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| Genotype |
MMTV-D1T286A
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| Species |
Mouse (Mus musculus)
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| Strain |
FVB
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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 |
Cyclin D1 levels are maintained at steady state by phosphorylation-dependent nuclear export and polyubiquitination by SCFFBX4-¿B crystallin. Inhibition of cyclin D1 proteolysis has been implicated as a causative factor leading to its overexpression in breast and esophageal carcinomas; however, the contribution of stable cyclin D1 to the genesis of such carcinomas has not been evaluated. We therefore generated transgenic mice wherein expression of either wild-type or a stable cyclin D1 allele (D1T286A) is regulated by MMTV-LTR.
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| Phenotype |
MMTV-D1T286A mice developed mammary adenocarcinomas at an increased rate relative to MMTV-D1 mice. Similar to human cancers that overexpress cyclin D1, D1T286A tumors were estrogen receptor-positive and exhibited estrogen-dependent growth. Collectively, these results suggest that temporal control of cyclin D1 subcellular localization and proteolysis is critical for maintenance of homeostasis within the mammary epithelium.
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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 |
caMOD, Curator
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| Principal Investigator / Lab |
Diehl*, JA.
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| Comment |
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| Model Availability: This model is available from |
| Strain |
Distributor |
Stock number |
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