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Recently, an article published in the internationally renowned commentaries Nature Reviews Molecular Cell Biology online reveals the IL31 stem cell niche. Stem cells exist in a specialized environment, known as the niche, and its ability to regulate stem cell characteristics and maintain the signal. Snapping a niche in physics in terms of the maintenance of stem cells is also very important, now Niola, who found ID (inhibitor of DNA binding) protein how to make neural stem cells to synchronize their niche in the IL32 stem and anchor. Mutant mice - the Id genes in neural stem cells in particular, knockout - will die within 24 hours after birth, and their proliferative ability of brain cells showed significantly reduced. Importantly, compared with control cells, neural stem cells to higher frequencies out of the cell cycle, stem cell compartment is also reduced. The culture of mutations in neural Il33 stem cells always have a severely impaired proliferation and self-renewal capacity, and premature differentiation. ID protein heterogeneous dimer with the basic helix - loop - helix (bHLH) transcription factor is an inhibition of DNA binding, at the same time Niola, who found encoding RAP1 a GTPase activating protein (RAP1GAP) gene as the ID protein is a direct goals. In the case of ID protein Rap1gap Il34 promoter is turned off, however, the lack of ID protein mutations in neural stem cells, to bHLH factor (with ID protein interactions) can Rap1gap promoter, and activation.

When neural stem cells were cultured in a media to promote their differentiation, the reduction in the loss of IL3RA stem cell markers and ID proteins, RAP1GAP increase, as well as the inhibition of RAP1 activity is consistent. In addition, the brain of knock Id mice showed abnormal expression of the ventricle region RAP1GAP, indicating that the ID inhibited the RAP1GAP expression of proteins in living organisms in order to maintain the activation of RAP1. RAP1 is a GTPase, known to regulate integrin signaling and the regulation of cell adhesion. Mutations in cultured stem cells is always a lack of ID protein, and therefore RAP1 activity, showing a reduction in focal adhesion, and can not adhere to the extracellular matrix (ECM) contains a layer of laminin or fibronectin. In addition, the adjustment of the Rap1gap RNA-silent fixes necessary for the ECM neural stem cell adhesion, indicating that the the ID-RAP1GAP-RAP1 path to stem cell adhesion to the ECM. Then reduced with the ID of the brain, RAP1GAP accumulation of the functional significance of what is it? Neural stem cells in the next ventricular zone dependent integrin contact with endothelial cells, thus constituting them to maintain the niche. ID proteins in embryonic and postnatal brain, neural stem cells to reduce the adhesion and the presence of nerve niche time every other room in the inactivation. Therefore, the ID of the-RAP1GAP-RAP1 path is necessary for neural stem cells anchored to their niche and to maintain the stem cell compartment. Further research will clarify the path of the ID-RAP1GAP-RAP1 function in stem cell manipulation to self-renewal and adhesion niche synchronization.