Good news comes here. USC researchers In Kyoung Mah from the lab of Francesca Mariani and colleagues at the University of California, San Diego, (UCSD) published a paper in the Stem Cell Reports. They describe a key gene in maintaining this critical balance between the results of producing too many and too few stem cells. The gene is called Prkci. It influences whether stem cells self-renew to produce more stem cells, or differentiate into more specialized cell types, such as blood or nerves.

The team conducted experiments by growing mouse embryonic stem cells, which lacked Prkci, into embryo-like structures in the lab. Without Prkci, the stem cells preferred self-renewal, and generated large numbers of stem cells, thus producing an abundance of secondary structures.

After careful inspection, the researchers found that stem cells lacking Prkci had many activated genes typical of stem cells, and some activated genes typical of cardiac, neural, and blood-forming cells. As a consequence, the loss of Prkci can also motivate stem cells to differentiate into the progenitor cells that form neurons, blood and heart muscle.

Prkci activates or deactivates a well-known group of interacting genes that are part of the "Notch signaling pathway to achieve the effects mentioned above. When Prkri is absent, the Notch pathway would produce a protein that signals to stem cells to make more stem cells. When Prkri is present, the Notch pathway just keeps silent and the stem cells all differentiate into specific cell types.

Their findings are good cues for the development of patient therapies. For example, patients with certain injuries or diseases may be benefit from them by using small molecule inhibitors to block the activity of Prkci, thus improve stem cell production. It will be wonderful to apply the findings to the case where stem cells are hard to generate. Flarebio offer high-quality recombinant proteins.