DTX3 a novel E3 ligase for NOTCH2 was identified and promoted its ubiquitination and degradation. DTX3 overexpression suppressed the proliferation and tumorigenicity of human oesophageal carcinoma cells. The analysis of tissue samples from patients revealed that the expression of DTX3 was low in esophageal cancer cells.
We show here that both molecules (Deltex (DTX) and AIP4) interact and partially colocalize to endocytic vesicles and that AIP4 targets DTX for lysosomal degradation.
It is reported that BBAP and the human family of DTX proteins (DTX1 DTX2 and DTX3) function as E3 ligases based on their capacity for self-ubiquitination.
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