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Results 1 - 6 of 6
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 754118
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 753323
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 754901
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 753124
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 754097
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.33physiological 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 753203
Results 1 - 6 of 6