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    Home > Active Ingredient News > Antitumor Therapy > Dev Cell: Scientists have found that PRC1 plays a role in genetic errors and cancer.

    Dev Cell: Scientists have found that PRC1 plays a role in genetic errors and cancer.

    • Last Update: 2020-07-30
    • Source: Internet
    • Author: User
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    The !---- excess protein PRC1, which is critical to cell division, is a clear sign of many cancer types, including prostate, ovarian and breast cancer.a new study published in The Journal of Developmental Cell in recent days shows that PRC1 acts as a "stick" in cell division, precisely controlling the rate at which two groups of DNA separate during a single cell division.findings could explain why too many or too few PRC1s can disrupt the process and lead to cancer-related genomic errors.PRC1 produces viscous friction, and resistance increases with speed.it produces friction similar to water."in the essence of DNA, motor proteins and microtubes, biology draws clues from physics.in the filamentphase phase of cell division, a single cell must copy its DNA into two identical collections and then quickly and effectively separate the DNA into two new socells.this is a physical behavior, and the cellular structure that does this is a filamented spindle, a machine that uses mechanical forces (push, pull, and resistance) to complete tasks.researchers believe that the force produced by PRC1 is to integrate and inhibit cell movement segregated with DNA separation, resulting in the correct rate of chromosomal separation.However, if the process goes wrong, the cells end up working with the wrong instruction manual, which can lead to uncontrollable growth of the cancer.focus: 1, there is a collection of fistriatal cross-linked protein PRC1 to produce friction 2, anti-microtube sliding scales and filament speed into a linear relationship 3, friction and PRC1 number of proportion, but not overlapping length or PRC1 density 4, PRC1 acts as a viscous damper, regulating the cell division in microtube velocity in split cells requires the assembly adjustment of spinning body equipment. the correct tissue of the microtubes inspindle is driven by a motor protein that exerts force sliding the filaments, rather than the motion protein, which crosses the filamentinto into a higher order, such as overlapping beams.it is not clear how the active and the forces are integrated to produce a regulated mechanical output within the spindle.here, the researchers used simultaneous optical capture and total internal reflex fluorescence (TIRF) microscopes to directly measure the friction against microtube sliding produced by the filamented crosslink protein PRC1.these forces are proportional to the microtube sliding speed and the number of PRC1 crosslinkings, but does not depend on the overlap length or the PRC1 density within the overlap.results show that PRC1 acts like a mechanical damper, producing significant resistance to rapid motion but minimal resistance to slow motion, thus integrating various movements into a mechanical result.the Forth laboratory to examine the physical forces applied by the components of the cell structure, such as a fission spindle.spindles are formed by two centers concentrated on the opposite side of two newly formed and desired identical chromosomal groups near the center of the cell.dense network of microspheres extends from the center to form cages around and connecting chromosomes.then, with the help of millions of proteins and motor proteins, the microtubes begin to shorten and slide, pulling the chromosomes toward the center until the two groups are separated.PRC1 is a "cross-linking agent", a long and elastic molecule with a head at both ends, connecting two microtubes along its length.near the center of the silk-splitted spindle body, a large number of PRC1s link microtubes into bundles.Forth's team created a controlled version of the microtubule sliding mechanism in the lab and used optical capture technology to measure the friction of THE PRC1 that slides between microtubes.optical capture relies on a tightly focused laser beam that attracts objects attached to a microtube (in this case, micro polystyrene beads).the researchers used laser beam pull beads (similar to the "traction beam" in science fiction) and converted refracted light into direct forces when the beadresists the pull of the trap.the team also marked PRC1 with fluorescent molecules so that they could observe the movement and distribution of microtubes when they were pulled apart.they used a full-reflection fluorescence microscope to collect experimental images while recording forces.forth and his colleagues found that as more and more proteins are added to the system, they encounter greater resistance as microtube movements accelerate.essentially, PRC1 behaves like glue that holds cells together.like many biological processes, without this protein, the cell is in trouble because it fails when it divides.everything in the cell is glued together, which may be the link between the protein and cancer.there is a balance in healthy cell division, which is to correctly and precisely control the right amount of the rate.limitations of the study: The limitation of the study is whether other non-motor proteins have been bundled and aggregated in spindles or granulated microtubes, such as NuMA or HURP, and produce similar viscosity forces to resist microtube sliding, or whether other mechanisms have been used, which remains to be seen. the study reveals the inner workings of the basic mechanisms of biology, providing the knowledge that will enable us to better fight cancer. this is a well-designed and well-designed study that lays the foundation for future anti-cancer strategies. data show that the collection of PRC1 molecules can produce resistance to relative microtube sliding. the size of these forces is proportional to the sliding rate and the total number of junctions, but not related to the density or overlapping length of the crosslinking agent. resistance to the linear proportional dependence of the sliding speed shows that the PRC1 group is represented as avicosatic joint agent. When stops sliding, the resistance relaxes, and restoring the sliding causes the resistance to be greater than the initial sliding event. finally, the researchers proposed a simple quantitative model that summarizes the key characteristics of the data by introducing parameters that allow the end of the microsphere to act as a partial reflexoee barrier against prC1 diffusion. the last article clarifies the mechanism by which PRC1 molecular aggregates can regulate the motion of microspheres within split cells. source: Immune Cell Research bioworld !-- content presentation ends - !-- determine whether the login ends.
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