echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Study of Nervous System > Neuron: Gene editing helps neurons extend their life.

    Neuron: Gene editing helps neurons extend their life.

    • Last Update: 2020-07-31
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    27 July 2020 // --- Most neurons are produced during embryonic development and are not "backed up" after birth.
    researchers generally agree that their survival rates are almost external, or by external forces, such as the tissues and cells that neurons provide to nerve cells.
    a team led by Sika Zheng, a biomedical scientist at the University of California, Riverside, challenged the concept and reported that the continued survival of neurons was inherently programmed during development.
    study, published in the journal Neuron, found a mechanism that the researchers say triggers when neurons are first produced, inherently reducing the occurrence of normal forms of cell death or apoptosis.
    when this genetic regulation stops, continuous neuronal survival is destroyed and animals die.
    (photo: www.pixabay.com) the survival of organisms, brain function and adaptability depend on the survival of their neurons.
    in higher organisms, neurons control breathing, eating, feeling, motor movement, memory, emotion and cognition.
    they can die from many unnatural causes, such as neurodegenerative diseases, injuries, infections and trauma.
    neurons are long-lived cells, but the genetic control that makes them live longer is unclear.
    Zheng's team now reports that at the heart of the mechanism spent on bak1, a apoptosis-promoting gene that activates it, leads to apoptosis.
    when this small fragment of genetic sequence is stitched together into the final Bak1 gene product, the expression of Bak1 is turned off.
    " apoptosis is a way to control the renewal of all post-life animal cells and tissue stability, and most non-nerve cells can easily respond to internal and external pressures and apoptosis.
    , however, the cells are tightly controlled in neurons so that they can survive for many years.
    We now show how the genetic attenuation of apoptosis occurs.
    " Zheng's team identified Bak1 microtopics through large-scale analysis of expression data from human tissue, mouse tissue, the developing brain, the developing forebrain of mice, and the developing brain in mice.
    the team first compared neural and non-neural tissues in humans and mice to identify neurospecific exons.
    , they found that cortical neurons reduced their sensitivity to apoptosis as early as they were born.
    they also found that apoptosis decreased during neuronal development before neurons established connections or nerves dominated other cells, suggesting that factors other than external signals may also play a role. "We've shown that neurons change the way they regulate cell death during development,"
    .
    this is necessary to ensure a long neuronand longevity and to maintain the integrity of the neural circuits of brain function.
    " (bioon.com) Source: Neuron s are all-en-genetically programmed to have long lives original origin: Lin et al, Developmental Attenuation of Neuron Apoptosis by Neural Specific-Splicing Bak 1 Microexon, Neuron (2020). DOI: 10.1016/j.neuron.2020.06.036.
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.