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Strain
B6.129S4-Ucp2tm1Lowl/J

Summary Data Summary
Official Name B6.129S4-Ucp2tm1Lowl/J
Common Name UCP2 KO
Description A targeting vector was created by replacing exons 3-7 of the
endogenous gene with a PGK-Neo expression cassette. This
construct was electroporated into 129S4/SvJae-derived J1
embryonic stem (ES) cells. Correctly targeted ES cells were
injected into C57BL/6 blastocysts and chimeric mice were
bred to C57BL/6. The resulting heterozygotes were
backcrossed to C57BL/6 mice for 10 generations before
arrival at the The Jackson Laboratory.
Development Status Phenotyping ongoing
Creation Method knockout
Breeding Type intercross
Phenotype Description Homozygous mice are viable and fertile and do not express
full length mRNA in heart, kidney, spleen, white adipose
tissue, and pancreatic islets. In splenic mitochondria,
endogenous protein was undetectable. When grown under high
glucose conditions, cultured pancreatic islet cells from
homozygous mice have increased insulin secretion and ATP
levels compared to wildtype. Homozygous mice have 18% lower
blood glucose levels. Whether fasting or fed, homozygotes
have approximately 3-fold greater serum insulin due to
increased insulin secretion. Similarly, glucose-stimulated
insulin secretion is significantly increased. High fat
diet-fed mice or palmitate-treated islets maintain
pancreatic glucose responsiveness in vivo and in vitro
compared to wildtype. Mitochondria isolated from the
dopaminergic mesencephalic nigral cells of homozygous mice
have increased reactive oxygen species but lesser
mitochondria number and increased sensitivity to MPTP,
mimicking Parkinson's disease.

In a recent study (Endocrinology, 2009, Epub Feb 26) it was
found that homozygous mutant mice exhibit increased
oxidative stress as well as impaired glucose-stimulated
insulin secretion, a finding that contrasts from the initial
phenotype description. In the publication, it was suggested
that the difference could be attributed to the earlier
studies being performed on mice with a mixed B6;129S4
genetic background. These later studies, mice on a congenic
B6.129S4 genetic background were used.

This mouse may be useful in studies of diabetes,
glucose-dependent metabolism-secretion coupling, aerobic
respiration, Parkinson,s disease, epilepsy, stroke, and
other neurodegenerative diseases.
TypeCount
Investigators 1
Genomics - Modifications 1
Experiments 2
Publications 1


Investigators
NameInstitution
Patty LeeYale University


Genomic Information
GeneAllele 1Allele 2Protocol
Ucp2knockoutknockoutNot Specified






PublicationAltmetricsSubmitted ByPubMed IDStatus
Endothelial uncoupling protein 2 regulates mitophagy and pulmonary hypertension during intermittent hypoxia.
Haslip M, Dostanic I, Huang Y, Zhang Y, Russell KS, Jurczak MJ, Mannam P, Giordano F, Erzurum SC, Lee PJ
Arteriosclerosis, thrombosis, and vascular biology, 2015 (35), 1166 - 78
Submitted Externally
25814675
Published

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