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Literature summary for 2.3.2.33 extracted from
- The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction (2013), Cell Rep., 3, 1422-1429 .
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | Q7TPH6 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| neuron | - |
Mus musculus | - |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | Phr1 E3 ubiquitin ligase is a central component of degeneration program that drives the loss of damaged axons. Loss of Phr1 results in prolonged survival of severed axons both in the peripheral and central nervous systems, as well as preservation of motor and sensory nerve terminals. Phr1 depletion increases the axonal level of the axon survival molecule nicotinamide mononucleotide adenyltransferase 2 (NMNAT2), and NMNAT2 is necessary to mediate Phr1-dependent axon stability | Mus musculus |
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Release 2023.1 (January 2023)
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