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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Ubiquitin protein ligase E3A

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. [provided by RefSeq, Jul 2008] (from NCBI)
Papers using UBE3A antibodies
TBL1 and TBLR1 phosphorylation on regulated gene promoters overcomes dual CtBP and NCoR/SMRT transcriptional repression checkpoints.
Xu Aimin, In PLoS ONE, 2007
... The rabbit polyclonal E6-AP antibody (A300–352A) was from Bethyl Laboratories ...
Papers on UBE3A
Dysfunction of the ubiquitin ligase Ube3a may be associated with synaptic pathophysiology in a mouse model of Huntington disease.
Jana et al., Gurgaon, India. In J Biol Chem, 2012
the loss of function of Ube3a might be associated with the synaptic abnormalities observed in HD.
Identification and proteomic analysis of distinct UBE3A/E6AP protein complexes.
Howley et al., Boston, United States. In Mol Cell Biol, 2012
proteomic studies reveal a level of complexity for E6AP that has not been previously appreciated and identify a number of new cellular proteins through which E6AP may be regulated or functioning
E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis.
Haupt et al., Melbourne, Australia. In Blood, 2012
E6AP expression is elevated in Burkitt lymphomas.
Maternal loss of Ube3a produces an excitatory/inhibitory imbalance through neuron type-specific synaptic defects.
Philpot et al., Chapel Hill, United States. In Neuron, 2012
This study demonistrated that Ube3a deficices mice product produces an excitatory/inhibitory imbalance through neuron type-specific synaptic in visual cortex.
Proteomic identification of E6AP as a molecular target of tamoxifen in MCF7 cells.
Trivedi et al., Lucknow, India. In Proteomics, 2012
Applied 2DE and MS based proteomics approach to identify target proteins of Tam. Show that Tam leads to inhibition of E6AP expression presumably by autoubiquitination, which leads to enhanced G0-G1 growth arrest and apoptosis.
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