ID:UBA3_HUMAN DESCRIPTION: RecName: Full=NEDD8-activating enzyme E1 catalytic subunit; EC=6.3.2.-; AltName: Full=NEDD8-activating enzyme E1C; AltName: Full=Ubiquitin-activating enzyme E1C; AltName: Full=Ubiquitin-like modifier-activating enzyme 3; Short=Ubiquitin-activating enzyme 3; FUNCTION: Catalytic subunit of the dimeric UBA3-NAE1 E1 enzyme. E1 activates NEDD8 by first adenylating its C-terminal glycine residue with ATP, thereafter linking this residue to the side chain of the catalytic cysteine, yielding a NEDD8-UBA3 thioester and free AMP. E1 finally transfers NEDD8 to the catalytic cysteine of UBE2M. Down-regulates steroid receptor activity. Necessary for cell cycle progression. ENZYME REGULATION: Binding of TP53BP2 to the regulatory subunit NAE1 decreases activity. PATHWAY: Protein modification; protein neddylation. SUBUNIT: Heterodimer of UBA3 and NAE1. Interacts with NEDD8, UBE2F and UBE2M. Binds ESR1 and ESR2 with bound steroid ligand (By similarity). Interacts with TBATA (By similarity). INTERACTION: P61081:UBE2M; NbExp=2; IntAct=EBI-717567, EBI-1041660; TISSUE SPECIFICITY: Ubiquitously expressed. MISCELLANEOUS: Arg-211 acts as a selectivity gate, preventing misactivation of ubiquitin by this NEDD8-specific E1 complex. SIMILARITY: Belongs to the ubiquitin-activating E1 family. UBA3 subfamily. SEQUENCE CAUTION: Sequence=AAC27648.1; Type=Erroneous initiation;
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q8TBC4
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.