BAIT
KBTBD4
BKLHD4, HSPC252
kelch repeat and BTB (POZ) domain containing 4
GO Process (0)
GO Function (0)
GO Component (0)
Homo sapiens
PREY
PSMD11
Rpn6, S9, p44.5
proteasome (prosome, macropain) 26S subunit, non-ATPase, 11
GO Process (24)
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]
- proteasome assembly [IMP]
- 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]
- stem cell differentiation [IMP]
- ubiquitin-dependent protein catabolic process [IMP]
- viral process [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Proximity Label-MS
An interaction is inferred when a bait-enzyme fusion protein selectively modifies a vicinal protein with a diffusible reactive product, followed by affinity capture of the modified protein and identification by mass spectrometric methods.
Publication
UM171 Preserves Epigenetic Marks that Are Reduced in Ex Vivo Culture of Human HSCs via Potentiation of the CLR3-KBTBD4 Complex.
Human hematopoietic stem cells (HSCs) exhibit attrition of their self-renewal capacity when cultured ex vivo, a process that is partially reversed upon treatment with epigenetic modifiers, most notably inhibitors of histone deacetylases (HDACs) or lysine-specific demethylase LSD1. A recent study showed that the human HSC self-renewal agonist UM171 modulates the CoREST complex, leading to LSD1 degradation, whose inhibition mimics the activity ... [more]
Cell Stem Cell Dec. 07, 2020; 28(1);48-62.e6 [Pubmed: 33417871]
Throughput
- High Throughput
Curated By
- BioGRID