EC Number   |
General Information |
Reference |
|---|
   6.3.2.19 | malfunction |
downregulation of IBRDC2 induces increased cellular levels and accumulation of the active form of Bax |
714828 |
| 6.3.2.19 | malfunction |
elevated expression of E3 ubiquitin ligases MuRF1 and MAFbx is involved in skeletal muscle protein breakdown in rats with thermal injury |
701635 |
| 6.3.2.19 | malfunction |
Huwe1 balances proliferation and neurogenesis in the developing brain which is subverted in malignant brain tumors |
703367 |
| 6.3.2.19 | malfunction |
mahogunin ring finger-1, MGRN1, is a RING domain-containing ubiquitin ligase mutated in mahoganoid, a mouse mutation causing coat color darkening, congenital heart defects, high embryonic lethality, and spongiform neurodegeneration. MGRN1 isoforms decrease MC1R and MC4R signaling to cAMP, without effect on beta2-adrenergic receptor and independently on receptor plasma membrane expression, ubiquitylation, internalization, or stability and occurred upstream of Galphas binding to/activation of adenylyl cyclase. Overexpression of Galpha5 abolishes the inhibitory effect of MGRN1 |
704571 |
| 6.3.2.19 | malfunction |
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 and prevents desensitization of capsaicin-induced calcium increases |
715640 |
| 6.3.2.19 | malfunction |
MURF3 knockdown in cardiomyocytes by an isogene-specific siRNA leads to upregulation of MURF2 expression. Knockdown of both MURF2 and MURF3 severely disrupts the formation of ordered Z- and M-bands, likely by perturbed tubulin dynamics. It is suggested that ubiquitin-mediated protein turnover and MURF2 in particular play an unrecognised role in the earliest steps of heart muscle differentiation, and that partial complementation of MURF2 deficiency is afforded by MURF3 |
714798 |
| 6.3.2.19 | malfunction |
selective genetic inactivation of Cbl-b E3 ligase activity (C373AKI/KI knock-in) phenocopies the T cell responses observed when total Cbl-b is ablated, resulting in T cell hyperactivation, spontaneous autoimmunity, and impaired induction of T cell anergy in vivo. Mice carrying a Cbl-b E3 ligase-defective mutation spontaneously reject tumor cells that express human papilloma virus Ags |
715795 |
| 6.3.2.19 | malfunction |
silencing of Mule stabilizes Miz1, thereby suppressing TNFalpha-induced JNK activation and cell death |
716752 |
| 6.3.2.19 | malfunction |
siRNA knockdown of MURF2 in neonatal rat cardiomyocytes disrupts posttranslational microtubule modification and myofibril assembly, and is only partly compensated by upregulation of MURF3 but not MURF1. It is suggested that ubiquitin-mediated protein turnover and MURF2 in particular play an unrecognised role in the earliest steps of heart muscle differentiation, and that partial complementation of MURF2 deficiency is afforded by MURF3 |
714798 |
| 6.3.2.19 | malfunction |
the knockdown of Fbxo45 in primary cultured hippocampal neurons results in a greater frequency of miniature excitatory postsynaptic currents |
715561 |
