![]() ![]() Using super-resolution microscopy, they observed that the scaffold function of BNIP-2 enables it to interact with a protein called LATS1, which binds to and sequesters YAP outside of the nucleus. In this case, the research team discovered that when the cardiac muscle genes were switched on, YAP was inactivated and prevented from entering the nucleus. These sets of “growth-promoting” genes will be turned off when YAP is sequestered out of the nucleus in the cytoplasm. When YAP is in the nucleus, it typically helps to turn on genes that promote cell and tissue growth by increasing cell number and size. YAP is a well-known mechanosensitive protein that moves in and out of the nucleus in response to mechanical signals. Conversely, inhibition of BNIP-2 expression resulted in alteration in various cardiac signalling pathways, specifically activation of targets of the YAP protein signalling pathway. those coding for cardiac muscle proteins that power heart contraction) correlated with increased expression of the BNIP-2 gene and protein. Previous work from the Low lab has shown that the BCH domains target members of the Rho protein family that act as molecular switches to regulate signalling pathways, and BNIP-2 scaffolding has been implicated in cell movement, growth, and skeletal muscle cell signalling.Īn initial genetic experiment revealed that increased expression of heart genes involved in force generation (i.e. The BCH domain is conserved, meaning it can commonly be found on other proteins. This scaffolding is achieved through a specific region on BNIP-2 termed the ‘BCH domain’. As the name suggests, scaffold proteins work by bringing together multiple proteins so they can interact. Given the integrative nature of the heart, the team focused on the signalling scaffold protein BNIP-2. This interdisciplinary study used a combination of genetic and biochemical approaches in conjunction with biophysical analysis and super-resolution microscopy imaging. Roger Foo (NUS Yong Yoo Lin School of Medicine). Pakorn Kanchanawong (Department of Biomedical Engineering) in partnership with consultant cardiologist Prof. Low Boon Chuan (Department of Biological Sciences and NUS College) and Assoc. Darren Wong, under the supervision of MBI Principal Investigators Assoc. The research team was headed up by MBI Research Scientist (and ex-MBI graduate student), Dr. To investigate the workings of the heart, an interdisciplinary team of scientists from the Mechanobiology Institute joined forces with clinicians from the Cardiovascular Research Institute, NUHS. The reverse needs to occur once the workout is finished. For instance, during a strenuous workout the heart may need to respond to a sudden rush of adrenalin hormones – a biochemical signal – by increasing the mechanical rate at which the heart is beating. Going back to the example of exercise we can see how the heart needs to interpret both biochemical and mechanical signals. One of the major challenges in this revolves around the unique function of the heart. Therefore, many researchers have sought to understand the mechanism by which muscle cells in the heart differentiate into specialised cardiac muscle to see if there may be a way to enhance cardiac muscle growth and regeneration. As damage accumulates over time from lifestyle factors, disease, or ageing, the heart will become progressively weaker and eventually fail. However, certain muscles have a limited regenerative potential once fully developed, such as the heart, despite the essential role it plays in constantly pumping blood around the body. Fortunately, most of our muscles have the ability to renew and regenerate from muscle stem cells, so getting back into shape can be done with exercise and effort. We all know how muscles lose definition when we don’t exercise for a period of time. ![]()
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