ORIGINThe RIPHAT transgene consists of a PCR-generated cDNA encompassing the h-IAPP coding sequence under the regulation of the rat insulin II promoter/5’untranslated region and followed by intron I from the human albumin gene and the polyadenylation site/RNA termination region from the human glyceraldehydes-3-phosphate gene. Hemizygotes of the RHF line described in Couce et al. (Pfizer) were self-crossed to generate F1 offspring. Transgenic offspring were identified by PCR amplification of RIPHAT from tail tissue. Transferred to Charles River under exclusive license in 2011.
STRAIN CODEComing Soon
MUTATION INFORMATIONThe islet in type 2 diabetes is characterized by a deficit in β-cell mass, increased β-cell apoptosis and impaired insulin secretion. In addition, the islets often contain deposits of islet amyloid, a protein derived from islet amyloid polypeptide (IAPP) that is co-secreted with insulin by β-cells. These proteins can form amyloid tendrils or oligomers which can initiate apoptosis. Animals with high levels of IAPP would be expected to develop diabetes due to the increased presence of the oligomers.
Rats and mice have similar IAPP homology but differ from humans by substitution of proline residues in the amyloidogenic portion of IAPP, and do not form amyloid tendrils or oligomers nor spontaneously develop diabetes in midlife. Thus, insertion of a human transgene, may provide a means to explore the role of oligomers in β-cell destruction.
Features of the Model
ORDERING INFORMATIONPlease call 1.800.LAB.RATS if you would like to place an order.
For additional information about Rip-HAT mice, please contact Technical Services at 1.877.CRIVER.1 (1.877.274.8371) or email@example.com.
DISCLAIMERRip-HAT mice may be subject to the licensed patents and are sold only for research purposes under agreement from Pfizer, Inc.
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