Cell: Special proteins may promote cells in stress states into molecular "traffic jams" that can trigger cell suicide paths.

August 9, 2020 // -- When cells experience high levels of stress (such as exposure to excessive ultraviolet radiation), the nucleucleus in the cells collides and causes "traffic jams" within the cells, and in a recent study published in the international journal Cell, scientists from Johns Hopkins University and others have found a special protein that identifies this "traffic" problem and pushes cells into suicide pathways;
Source: National Institute of Health 3D Print Exchange Researcher Dr Rachel Green says we have long studied how cells identify problems in coded information and how the process relies on ucucose bodies, which can be caused by errors in genome coding or damage to cells caused by the environment.
The work of
RNA along mRNA is to decode mRNA and provide a set of instructions to make proteins, and when cell pressure increases, the mRNAs are damaged and the rna cannot travel along the mRNA, so that it collides with each other like a molecular bump, because the rna does not reach the end of the mRNA, resulting in incomplete proteins.
Incomplete proteins are aggregated and cause disease, so cells need to block the production and aggregation of this incomplete protein; when there are few collisions between nucleomers, cells are usually able to recover, and cells initiate a path called integrated stress response (ISR) to ensure that cells are protected from death; However, if a collision results in a serious "traffic accident", the cells trigger a stress response in the nucleosome, which promotes cell suicide; the researchers wanted to use research to clarify how cells assess their internal "traffic conditions" and how to lock in these mitochondrial collisions, and then added an antibiotic in the lab to block the movement of the nucleic glycosomes into mammalian cells.
In the undressed cells, the researchers did not find a problem with the "traffic flow" of the cleaccharides, and under the effect of high doses of antibiotics, they found that the ucucose body stopped moving together completely, but when the scientists treated the cells with a medium dose of antibiotics, they observed the occurrence of ucucol collisions in the cells, making them feel strange that the proteins involved in promoting the integrated stress response of life and promoting the stress response of the dead cytone were activated.
researchers say they have identified a key protein called ZAK, which is part of the MAP3K family protein, which binds to the colliding nucleosis and activates itself.
Next, researchers will continue to delve deeper, using cryogenic electron mirror technology to create ZAK's 3D structure to clarify the exact location/location of its binding to the uccosos, and to clarify how different cell types become more or less susceptible to the collision of the ucuclyces.
finally, the researchers say that when cells are under stress in a healthy and diseased state, we may be expected to use special drugs to target THEK-mediated molecular paths to change the fate of cells.
() Original sources: Colin Chih-Chien Wu, Amy Peterson, Boris Zinshteyn, et al. Ribosome Collisions General Responses to Regulate Cell Cell (2020). Doi: 10.1016/j.cell.2020.06.006.