receive those messages as they arrive, SH2B1’s partnership with JAK2 is an important one. In a previous paper, Rui and his former mentor and current colleague Christin Carter-Su, Ph.D., showed that SH2B1 encourages the action and production of JAK2, unlike two other proteins that have been shown by other teams to reduce its activity. Carter-Su is a professor of molecular and integrative physiology and heads the biomedical research division of the Michigan Diabetes Research and Training Center.
In addition to revealing the importance of SH2B1 activity in the brain, the new paper shows that SH2B1 is expressed in four different forms in many tissues of the body, including fat cells known as adipose tissue, as well as the liver, heart, pancreas and muscle.
Rui and his team also explored the role of SH2B1 in fat cells, finding that the knockout mice that lacked the SH2B1 gene stored away much more fat than normal mice, and had much larger fat cells – giving them two-and-a-half times more body fat content than normal mice. The mice that had some of their SH2B1 restored in just their brains by genetic alteration did not experience this – and in fact had less fat than normal mice.
Since these mice lacked the ability to make SH2B1 in their fat cells, the authors suspect that fat-cell SH2B1 encourages the storing of fat. When they tested this theory, they found that SH2B1 appeared to help mouse embryonic cells turn into fat cells, a process called adipogenesis. But, they suspect, the action of SH2B1 in the brain trumps its action in fat tissue, leading to the development of obesity in mice that lack SH2B1 in both locations.
Rui and his team now hope to explore SH2B1's role in the brain and body even further, and hope to translate their findings into clinical research involving humans. They hope that their findings will help lead to better tactics for understanding the causes of obesity and its consequences, including Type 2Page: 1 2 3 4 Related medicine news :1
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