2.3.2.33: RCR-type E3 ubiquitin transferase
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For detailed information about RCR-type E3 ubiquitin transferase, go to the full flat file.
Reaction
Synonyms
E3 ubiquitin-protein ligase, MYCBP2, PHR1, RPM-1
ECTree
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General Information
General Information on EC 2.3.2.33 - RCR-type E3 ubiquitin transferase
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physiological function
loss of E3 ubiquitin ligase MYCBP2 causes the up-regulation of small GTPase Ran and GTPase-activating protein RanGAP1 in dorsal root ganglia under basal conditions and during inflammatory hyperalgesia. SUMOylated RanGAP1 physically interacts with MYCBP2 and inhibits its E3 ubiquitin ligase activity. Stimulation of neurons induces a RanGAP1-dependent translocation of MYCBP2 to the nucleus. In the nucleus of in dorsal root ganglia neurons MYCBP2 co-localizes with Ran and facilitates through its RCC1-like domain the GDP/GTP exchange of Ran. The nuclear localization of Ran is strongly increased in MYCBP2-deficient dorsal root ganglia
physiological function
loss of MYCBP2 in peripheral sensory neurons inhibits the internalization of transient receptor potential vanilloid receptor 1 (TRPV1) in a p38 MAPK-dependent manner. This prevents desensitization of activity-induced calcium increases and prolongs formalin-induced thermal hyperalgesia
physiological function
Magellan mutant embryos, having a truncated Phr1 protein, motor axons are error prone and wander inefficiently at choice points within embryos. Motor and sensory neurons from Magellan mutants display abnormal morphologies due to a breakdown in the polarized distribution of components that segregate between axons and growth cones. The Magellan phenotype can be reversed by stabilizing microtubules with taxol or inhibiting p38-MAPK activity
physiological function
mice heterozygous for either Mycbp2 or receptor Robo2 are normal, mice double heterozygous for the two genes produce defects in dorsoventral topography in the olfactory bulb. Loss of Mycbp2 function leads to the loss of molecular identity of a subpopulation of olfactory sensory axons that normally express ROBO2. In addition, double heterozygous mice show complete absence of the hippocampal commissure
physiological function
mice with a MYCBP2-deficiency in peripheral sensory neurons show prolonged thermal hyperalgesia. Loss of MYCBP2 constitutively activates p38 MAPK and increases expression of several proteins involved in receptor trafficking. Loss of MYCBP2 inhibits internalization of transient receptor potential vanilloid receptor 1 (TRPV1) and prevents desensitization of capsaicin-induced calcium increases
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