New progress has been made in stress regulation of neuron endologic network stress.

Endoenstrucing stress occurs under a variety of physiological and pathological conditions, especially in some neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Peme's disease, etc.
present, endosurcing stress research is generally carried out in the pattern of drug or physical (thermal) stimulation causing acute endosurge stress response.
, however, this acute, intense endotrogenic network stress is rare in neurodegenerative diseases, and endotrogen network stress caused by drug stimulation occurs in a variety of cells and is not neuron-specific.
, it is imperative to establish neuron-specific endotrogen network stress mode and carry out research on the mechanism of chronic endotogene network stress response.
Ding Mei research team of the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences found that four cross-membrane electrosynact proteins were expressed in D-type motor neurons, which can activate endoblast stress responses independently of cells.
addition, in combination with fluorescent markers, changes in the positioning of electrosyntic proteins indicate the occurrence of endosurgen network stress reactions.
the system can monitor neuron endosurance stress without the need for drugs or any other external stimuli.
Based on this system, genetic screening and biochemical mechanism studies have found that PMK-3, a member of the P38 MAPK family, regulates the classic IRE-1-XBP-1 endosurgency stress path through the direct phosphate endosurgen network stress signaling molecule IRE-1.
interestingly, insulin signaling pathways are transcriptied through cell autophagy rather than companion proteins (such as hsp-4), antagonists of endostrophic network stress mediated by the p38-IRE1-XBP1 pathway.
These results reveal the complex regulatory path of neuron-specific chronic endologic stress stress, which is of significance for clarifying how neurons deal with chronic endotrine stress caused by mutation or excessive protein accumulation, and provide clues to understanding the occurrence and development of related degenerative neuropathy.
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