
pmid: 11414708
C-cell tumors occur frequently (50%) in old WAG/Rij rats. Interestingly, genetically transmitted loss of CT binding sites in the kidney has also been demonstrated in WAG/Rij rats. To determine if these issues are resulted from mutation of calcitonin receptor (CTR), we analyzed the CTR genomic abnormality in WAG/Rij rat. We demonstrated that both Wistar and WAG/Rij rats expressed type-C1a CTR by RT-PCR analysis and their mRNA expressions were approximately equal by Northern blotting analysis. Direct sequence of RT-PCR products for CTR showed no different nucleotide sequences between the two strains. There were three polymorphisms at the first transmembrane domain and the fourth intracellular membranes, which are different from Sprague-Dawley rat. We concluded that the loss of CT binding in WAG/Rij rat is not related to CTR gene abnormality. Abnormal system of CTR amino acid modification may be occurred in WAG/Rij rat.
Calcitonin, Binding Sites, Polymorphism, Genetic, Protein Conformation, DNA Mutational Analysis, Membrane Proteins, Receptors, Calcitonin, Rats, Rats, Sprague-Dawley, Mutation, Animals, Female, RNA, Messenger, Rats, Wistar
Calcitonin, Binding Sites, Polymorphism, Genetic, Protein Conformation, DNA Mutational Analysis, Membrane Proteins, Receptors, Calcitonin, Rats, Rats, Sprague-Dawley, Mutation, Animals, Female, RNA, Messenger, Rats, Wistar
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