• Background: UTS2R is a highly-affinity UTS2 receptor that is activated by G protein-coupling through the phosphatidylinositol-calcium signaling pathway. It participates in the positive regulation of the circadian sleep/wake cycle, the regulation of rapid eye movement sleep (REM) and arousal. It regulates blood pressure by increasing the excretion of sodium and water, thereby lowering blood pressure.
• Targeting strategy: The exons 1 of the mouse Uts2r gene that encode the full-length protein and 3’UTR were replaced by human UTS2R exons 3 in B-hUTS2R mice. The promoter and 5’UTR region of the mouse gene are retained. The human UTS2R expression is driven by the endogenous mouse Uts2r promoter, while the mouse Uts2r gene transcription and translation will be disrupted.
• Validation: Human UTS2R mRNA was only detectable in homozygous B-hUTS2R mice but not in wild-type mice.
• Application: UTS2R may have a pro-inflammatory effect in the coronary artery lesions of Kawasaki disease.

Gene targeting strategy for B-hUTS2R mice. The exons 1 of the mouse Uts2r gene that encode the full-length protein and 3’UTR were replaced by human UTS2R exons 3 in B-hUTS2R mice. The promoter and 5’UTR region of the mouse gene are retained. The human UTS2R expression is driven by the endogenous mouse Uts2r promoter, while the mouse Uts2r gene transcription and translation will be disrupted.

Strain specific analysis of UTS2R mRNA expression in wild-type C57BL/6N mice and B-hUTS2R mice by RT-PCR. Skeletal muscle RNA were isolated from wild-type C57BL/6N mice (+/+) and homozygous B-hUTS2R mice (H/H), then cDNA libraries were synthesized by reverse transcription, followed by PCR with mouse or human UTS2R primers. Mouse Uts2r mRNA was only detectable in wild-type mice. Human UTS2R mRNA was only detectable in homozygous B-hUTS2R mice but not in wild-type mice.