The mortality of MOP3 deficient mice with a systemic functional failure.
MOP3 (also known as BMAL1), a master regulator of circadian rhythm, plays important roles in the regulation of cell differentiation and general physical functions. In the present studies, MOP3 deficient mice had significantly reduced body weight and showed remarkable mortality around six months of age. The levels of AST, ALT, BUN, or UREA in the blood of about four month-old MOP3(-/-) mice were significantly higher than MOP3(+/-) or MOP3(+/+) littermates. However, no apparent pathological changes in the livers, hearts, lungs or kidneys of about four month-old MOP3(-/-) mice were observed. In addition, altered levels of white blood cells, lympgocytes, and platelets in peripheral blood of MOP3(-/-)mice were detected. The results presented herein with MOP3-deficient mice offered the basic principle for the essential roles of MOP3 in keeping normal survival abilities in mice. This study may have significant clinical impacts on the consideration about the abnormality of circadian rhythms and sleeping disorders caused physical and metabolism dysfunctions as well as the mortality.[1]References
- The mortality of MOP3 deficient mice with a systemic functional failure. Sun, Y., Yang, Z., Niu, Z., Wang, W., Peng, J., Li, Q., Ma, M.Y., Zhao, Y. J. Biomed. Sci. (2006) [Pubmed]
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