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    Home > Biochemistry News > Biotechnology News > De-ubibinase axin-3 regulates the pattern of DNA damage response to the important kinase Chk1.

    De-ubibinase axin-3 regulates the pattern of DNA damage response to the important kinase Chk1.

    • Last Update: 2020-09-13
    • Source: Internet
    • Author: User
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    Genomic DNA continues to be attacked by DNA damage from a variety of sources, such as UVs in the natural environment, ROS produced by normal metabolism, etc.
    to maintain genomic stability, the ethyrocys have evolved a protective mechanism, the DNA damage response.
    DNA damage response is a complex signal transductive network system that senses DNA damage and transmits signals, which in turn causes a series of responses, such as cell cycle test points, DNA repair, transcription changes, and cell death when the damage is too severe.
    Chk1 is a key kinase in the genomic stability regulatory system and plays a key role in cell cycle testing, DNA repair, and cell survival.
    The Tang Tieshan Research Group of the National Key Laboratory of Membrane Biology of the Institute of Zoology of the Chinese Academy of Sciences found that the disease protein ATX3 of type 3 spinal cord congenerative disorder (SCA3/MJD1) is an important regulator of chk1 kinase stability.
    ATX3 deficiency can lead to a significant decrease in Chk1 protein levels, defects in chk1-mediated G2/M test points, and increased sensitivity to DNA damage.
    further studies have found that ATX3, as a de-ubibinase, can antagonize the E3 connective enzyme complex DDB1/CUL4A and FBXO6-mediated Chk1 multi-ubitin and degradation.
    ATX3's regulation of Chk1 stability is dynamic.
    rest state and replication pressure early on, the ATX3 binds to Chk1 and promotes its stability.
    long-term replication pressure, ATX3 and Chk1 are dissophased, along with the combination of Chk1 and E3 connective enzyme complex components.
    E3 connective enzymes to mediate Chk1 multi-ubilinization and degradation, facilitating the termination of test points, cell cycle recovery, and cell survival.
    the study not only found that ATX3 played an important role in the maintenance of genomic stability by regulating Chk1, but also helped to clarify the molecular pathological mechanisms of type 3 spinal cord coencephalopathy disorders.
    similar to Parkinson's disease, the main pathological feature of type 3 spinal cord co-optic disorder is the loss of dopamine-energy neurons, the pathological mechanism of which is not yet known.
    is important to explore the role of DNA injury response in dopamine neuron degeneration.
    study was published online February 9 in Nucleic Acid Research under the title ATX3 promotes genome integrity by stabilizing Chk1.
    The first authors of this article are Tu Yingfeng, a doctoral student, Liu Hongmei, an assistant researcher, and Zhu Xuexuan, a doctoral student, and Tang Tieshan, a researcher at the Institute of Animals, and Guo Caixia, a researcher at the Beijing Genomics Research Institute of the Chinese Academy of Sciences.
    the project was funded by the Ministry of Science and Technology and the Fund Committee.
    .
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