These NOD mice are hemizygous for the Lymphocytic choriomeningitis virus nucleoprotein under the control of human insulin promoter (HIP). This model provides a novel autoantigen expressed in pancreatic islet cells. LCMV infected transgenic mice provide an inducible system of early onset diabetes.
Dr. Matthais von Herrath, La Jolla Institute for Allergy and Immun
Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) under the control of the human insulin promoter (HIP). RT-PCR analysis indicates that transgenic mice express LCMV-nucleoprotein in the pancreas and thymus. Naive transgenic female mice exhibit slightly accelerated diabetes onset (95% diabetic by 35 weeks of age) when compared to wildtype controls (80% diabetic by 35 weeks of age), with no significant difference in overall diabetes incidence by 40 weeks of age. Immunohistochemistry of pancreas at one-week post LCMV infection shows an early infiltration of CD8 T cells in transgenic mice. Within 2 weeks of infection with LCMV HIP-NP mice exhibit rapid onset of diabetes compared to 6-8 months in infected B6.RIP-NP (Stock No. 004826) mice. LCMV infected transgenic mice exhibit upregulation of CXCR3 and CXCR10. This model provides a novel autoantigen expressed in pancreatic islet cells. LCMV infected transgenic mice provide an inducible system of early onset diabetes. This LCMV inducible strain may provide a model for early onset diabetes.
NOD/ShiLt-Tg(INS-NP)6171Mvh/J expresses the complete cDNA from Armstrong's clone 53b of the lymphocytic choriomeningitis virus, LCMV, nucleoprotein, NP, regulated by human insulin promoter, INS, commonly referred to as HIP. A Hepatitis B Virus polyadenylation signal as a terminator of transcription was fused downstream of the LCMV-NP. This transgene was microinjected into NOD/ShiLt oocytes and progeny of founder 6171, have been maintained on the NOD/ShiLtJ (Stock No. 001976) background (Martinic et al, 2007). In 2010, this strain arrived at The Jackson Laboratory and was backcrossed to NOD/ShiLtJ.
|Expressed Gene||NP, lymphocytic choriomeningitis virus nucleoprotein, viral|
|Site of Expression|
|Allele Name||transgene insertion 6171, Matthias von Herrath|
|Allele Type||Transgenic (Inserted expressed sequence)|
|Allele Synonym(s)||Ins-LCMV-NP; LCMV-NP|
|Gene Symbol and Name||Tg(INS-NP)6171Mvh, transgene insertion 6171, Matthias von Herrath|
|Promoter||INS, insulin, human|
|Expressed Gene||NP, lymphocytic choriomeningitis virus nucleoprotein, viral|
|Strain of Origin||NOD/ShiLt|
|Molecular Note||The transgene expresses the complete cDNA from Armstrong's clone 53b of the lymphocytic choriomeningitis virus, LCMV, nucleoprotein, NP, regulated by human insulin promoter, INS. A Hepatitis B Virus polyadenylation signal as a terminator of transcription was fused downstream of the LCMV-NP. This transgene was microinjected into NOD/ShiLt oocytes and founder line 6171 was maintained on the NOD/ShiLt background.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of
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