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
PCNA
ATLD2
proliferating cell nuclear antigen
GO Process (18)
GO Function (8)
GO Component (9)
Gene Ontology Biological Process
- DNA repair [TAS]
- DNA strand elongation involved in DNA replication [TAS]
- G1/S transition of mitotic cell cycle [TAS]
- base-excision repair [TAS]
- cell proliferation [TAS]
- epithelial cell differentiation [IEP]
- leading strand elongation [IBA]
- mismatch repair [IDA]
- mitotic cell cycle [TAS]
- nucleotide-excision repair [TAS]
- nucleotide-excision repair, DNA gap filling [TAS]
- positive regulation of deoxyribonuclease activity [IDA]
- regulation of transcription involved in G1/S transition of mitotic cell cycle [TAS]
- telomere maintenance [TAS]
- telomere maintenance via recombination [TAS]
- telomere maintenance via semi-conservative replication [TAS]
- transcription-coupled nucleotide-excision repair [TAS]
- translesion synthesis [IDA]
Gene Ontology Molecular Function- DNA polymerase binding [IPI]
- DNA polymerase processivity factor activity [IBA]
- MutLalpha complex binding [IDA]
- dinucleotide insertion or deletion binding [IDA]
- identical protein binding [IPI]
- protein binding [IPI]
- purine-specific mismatch base pair DNA N-glycosylase activity [IDA]
- receptor tyrosine kinase binding [IPI]
- DNA polymerase binding [IPI]
- DNA polymerase processivity factor activity [IBA]
- MutLalpha complex binding [IDA]
- dinucleotide insertion or deletion binding [IDA]
- identical protein binding [IPI]
- protein binding [IPI]
- purine-specific mismatch base pair DNA N-glycosylase activity [IDA]
- receptor tyrosine kinase binding [IPI]
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