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Negative regulation of Tkv by Ube3a was conserved in mammalian cells. These results reveal a critical role for Ube3a in regulating NMJ synapse development by repressing BMP (zeige TGFb ELISA Kits) signaling. This study sheds new light onto the neuronal functions of UBE3A and provides novel perspectives for understanding the pathogenesis of UBE3A-associated disorders.
Data indicate that E3 ligase called ube3 (dube3a) is required for brain development as mutants have defective mushroom bodies.
Rpn10 is targeted for degradation by Ube3a.
In Drosophila melanogaster the human homologue ube3a regulates the actin cytoskeleton and neuronal homeostasis.
MeCP2 and E6AP play a role in the transcriptional control of common target gene expression.
Ube3a regulates serotonin and dopamine synthesis in the fly brain by increasing GTP cyclohydrolase I (zeige GCH1 ELISA Kits) activity.
dube3a null mutants appear normal externally, but display abnormal locomotive behavior and circadian rhythms, and defective long-term memory; overexpression in the nervous system caused locomotion defects, dependent on the ubiquitin ligase activity
Overexpression of dUBE3A decreased dendritic branching.
study has broad implications for human disorders associated with UBE3A gain or loss of function and suggests that dysfunctional UBE3A might affect additional proteins and pathways that are sensitive to proteasome activity
We found that KD of E6AP attenuates cancer cell growth by promoting cellular senescence in vivo, which correlates with restoration of tumor suppression by PML (zeige PML ELISA Kits).
HCV core protein inhibits E6AP expression via DNA methylation to protect itself from ubiquitin-dependent proteasomal degradation and stimulate virus propagation.
E6AP suppresses breast cancer metastasis by regulating actin cytoskeleton remodeling through the control of ECT2 (zeige ECT2 ELISA Kits) and Rho GTPase (zeige RACGAP1 ELISA Kits) activity.
Dube3a is neither imprinted nor preferentially expressed from the maternal allele in fly neurons.
The ubiquitylation of beta-catenin by E6AP was dependent on its E3 ubiquitin ligase activity, but it was proteasome-independent and did not require HPV16-E6.
All patients with Angelman syndrome based on a deletion had epilepsy. Epilepsy was present in 3/4 children with UBE3A mutation. Laughter-induced postural muscle tone loss occurred only among deletion cases
The results of Trans-well and cell scratch tests showed that when ANCR expression was decreased, the invasion and migration abilities of SW620 cells significantly declined (both P < 0.05). In conclusion, these results suggest that lncRNA-ANCR could influence the invasion and migration of CRC (zeige CALR ELISA Kits) cells by specifically binding to EZH2 (zeige EZH2 ELISA Kits).
There were total 55 molecularly confirmed Angelman syndrome(AS) between January 1995 to September 2015 for review. 65.5% of them were caused by maternal microdeletion, 10.9% by paternal uniparental disomy, 3.6% by imprinting center defect and 14.5% by UBE3A gene mutation
The observation of Dup15q syndrome in individuals with maternally but not paternally inherited duplications of chromosome 15q11-q13, suggest that UBE3A drives the Angelman syndrome phenotype in this disorder. (Review)
Our findings suggest that UBE3A may act locally to regulate individual synapses while also mediating global, neuronwide influences through the regulation of gene transcription
treatment of topotecan, a brain-penetrating topoisomerase 1 (zeige TOP1 ELISA Kits) inhibitor, to HD transgenic mouse considerably improved its motor behavioural abnormalities. Finally, we show that topotecan treatment to HD mouse not only inhibits the expression of transgenic mutant huntingtin (zeige HTT ELISA Kits), but also at the same time induces the expression of Ube3a
We report that mice with maternally-inherited deletions of Ube3a that models Angelman syndrome show an increased social preference/interaction.
increasing UBE3A in the nucleus downregulates the glutamatergic synapse organizer Cbln1 (zeige CBLN1 ELISA Kits), which is needed for sociability in mice
Based on our findings, we propose that imprinting of UBE3A does not function to reduce the dosage of UBE3A in neurons but rather to regulate some other, as yet unknown, aspect of gene expression or protein function
the role of UBE3A is investigated in neurite contact guidance during neuronal development, is reported.
Results substantiate GABAergic Ube3a loss as the principal cause of circuit hyperexcitability in Angelman syndrome mice, lending insight into ictogenic mechanisms in AS.
Loss of Ube3a from tyrosine hydroxylase (zeige TH ELISA Kits)-expressing neurons impairs mesoaccumbal, non-canonical GABA co-release and enhances reward-seeking behaviour measured by optical self-stimulation.
Results suggest that the phenotypes observed in Angelman syndrome mice may be modulated by factors independent of Ube3a genotype
UBE3A dampens ERK (zeige EPHB2 ELISA Kits) pathway signalling in HPV E6 transformed HeLa cells
In the skeletal muscle of neonate pigs, both NECD (zeige NDN ELISA Kits) and SNRPN (zeige SNRPN ELISA Kits) were maternally imprinted, while UBE3A was not imprinted.
This gene encodes an E3 ubiquitin-protein ligase, part of the ubiquitin protein degradation system. This imprinted gene is maternally expressed in brain and biallelically expressed in other tissues. Maternally inherited deletion of this gene causes Angelman Syndrome, characterized by severe motor and intellectual retardation, ataxia, hypotonia, epilepsy, absence of speech, and characteristic facies. The protein also interacts with the E6 protein of human papillomavirus types 16 and 18, resulting in ubiquitination and proteolysis of tumor protein p53. Alternative splicing of this gene results in three transcript variants encoding three isoforms with different N-termini. Additional transcript variants have been described, but their full length nature has not been determined.
ubiquitin protein ligase E3A
, drosophila angelman syndrome
, angelman syndrome
, ubiquitin protein ligase E3A (human papilloma virus E6-associated protein, Angelman syndrome)
, ubiquitin-protein ligase E3A
, ubiquitin-protein ligase E3A-like
, CTCL tumor antigen se37-2
, E6AP ubiquitin-protein ligase
, human papilloma virus E6-associated protein
, human papillomavirus E6-associated protein
, oncogenic protein-associated protein E6-AP
, renal carcinoma antigen NY-REN-54
, E6-AP ubiquitin protein ligase
, ubiquitin conjugating enzyme E3A