BAIT
DDRGK1
C20orf116, UFBP1, dJ1187M17.3
DDRGK domain containing 1
GO Process (1)
GO Function (2)
GO Component (1)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
PSMD2
P97, RPN1, S2, TRAP2
proteasome (prosome, macropain) 26S subunit, non-ATPase, 2
GO Process (21)
GO Function (1)
GO Component (7)
Gene Ontology Biological Process
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [TAS]
- G1/S transition of mitotic cell cycle [TAS]
- RNA metabolic process [TAS]
- anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process [TAS]
- antigen processing and presentation of exogenous peptide antigen via MHC class I [TAS]
- antigen processing and presentation of exogenous peptide antigen via MHC class I, TAP-dependent [TAS]
- antigen processing and presentation of peptide antigen via MHC class I [TAS]
- apoptotic process [TAS]
- cellular nitrogen compound metabolic process [TAS]
- gene expression [TAS]
- mRNA metabolic process [TAS]
- mitotic cell cycle [TAS]
- negative regulation of apoptotic process [TAS]
- negative regulation of ubiquitin-protein ligase activity involved in mitotic cell cycle [TAS]
- positive regulation of ubiquitin-protein ligase activity involved in mitotic cell cycle [TAS]
- protein polyubiquitination [TAS]
- regulation of apoptotic process [TAS]
- regulation of cellular amino acid metabolic process [TAS]
- regulation of ubiquitin-protein ligase activity involved in mitotic cell cycle [TAS]
- small molecule metabolic process [TAS]
- viral process [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Affinity Capture-MS
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.
Publication
UFMylation maintains tumour suppressor p53 stability by antagonizing its ubiquitination.
p53 is the most intensively studied tumour suppressor1. The regulation of p53 homeostasis is essential for its tumour-suppressive function2,3. Although p53 is regulated by an array of post-translational modifications, both during normal homeostasis and in stress-induced responses2-4, how p53 maintains its homeostasis remains unclear. UFMylation is a recently identified ubiquitin-like modification with essential biological functions5-7. Deficiency in this modification leads ... [more]
Nat Cell Biol Dec. 01, 2019; 22(9);1056-1063 [Pubmed: 32807901]
Throughput
- High Throughput
Curated By
- BioGRID