UT Southwestern Medical Center at Dallas researchers have shown that the absence of a key oxygen-sensing molecule can lead to multiple developmental defects - from an enlarged heart to eye problems.
The researchers generated the first mouse model that lacks entirely a member of an important family of proteins involved in sensing hypoxia, a state of reduced oxygen in the bodys cells that is associated with conditions such as heart attacks, stroke and lung disease.
This new model allowed the scientists to take a closer look into the exact physiologic function of these proteins, which was unknown until now, and the model provided clues as to what human diseases may be caused by alterations in these proteins. The researchers reported in the online version of Nature Genetics that the absence of this crucial oxygen-sensing molecule leads to developmental defects due to the inability of the mice to respond to high, damaging levels of oxygen-based molecules called reactive oxygen species.
Amy Shields | UT Southwestern
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