Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 13, 2025 2 hours, 14 minutes ago
Medical News: Scientists from the Interdisciplinary Research Center on Biology and Chemistry at the Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, together with the University of Chinese Academy of Sciences in Beijing and the Key Laboratory of CNS Regeneration at Jinan University in Guangzhou, have uncovered a key molecular switch that controls how nerve fibers survive after injury. Their findings shed light on why damaged nerves deteriorate so quickly and point to a promising new strategy for slowing or preventing nerve degeneration.
New Protein Target Could Boost Nerve Repair
A Breakthrough in Understanding Axon Degeneration
When nerves are cut or damaged, the part of the nerve separated from the cell body begins to break apart in a process known as Wallerian degeneration. Until now, scientists knew that a protein called NMNAT2 plays a crucial role in keeping nerve fibers alive but also understood that it disappears very rapidly after injury. This
Medical News report reveals why that happens and identifies a protein called FBXO21 as the key regulator that marks NMNAT2 for destruction.
Through a series of detailed laboratory studies, the researchers showed that FBXO21 attaches tiny molecular tags, known as ubiquitin, onto NMNAT2. These tags signal the cell to break NMNAT2 down, reducing its levels and triggering the degeneration process. Importantly, when FBXO21 was removed or blocked, NMNAT2 remained at higher levels, and nerve fibers survived significantly longer after injury.
Key Study Findings Show FBXO21 Drives Nerve Breakdown
The team discovered that FBXO21 forms part of a larger protein complex, known as the SCFFBXO21 complex, which is responsible for selecting NMNAT2 for degradation. They pinpointed a specific location on NMNAT2, a site called K155, where this tagging occurs. By creating a special version of NMNAT2 that cannot be tagged at this position, the researchers produced a much more stable form of the protein. This modified NMNAT2 lasted far longer inside cells and was even more effective at protecting nerve fibers after injury.
Mouse experiments reinforced the laboratory findings. Animals genetically engineered to lack FBXO21 showed much higher NMNAT2 levels in their nerves and experienced dramatically slower nerve degeneration after injury. Injured nerves in these mice remained intact long after nerves in normal mice had broken down.
Implications for Nerve Injury and Neurodegenerative Diseases
These findings suggest that blocking FBXO21 or preventing NMNAT2 degradation could become a powerful approach for treating nerve injuries and possibly slowing diseases that involve nerve fiber loss. Because NMNAT2 stability appears essential for nerve survival, therapies that keep this protein active may offer new hope for conditions such as peripheral neuropathy, spinal cord injuries, and even early-stage neurodegenerative disorders. While more testing is needed, this study provides one of the clearest targets yet for preserving nerve health and slowing destructive nerve processes. This work opens the door
to future treatments that could help millions affected by nerve damage worldwide.
The study findings were published in the peer reviewed Journal of Cell Biology.
https://rupress.org/jcb/article/224/11/e202501072/278344/SCFFBXO21-mediated-ubiquitination-and-degradation
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