BAIT
DOT1L
DOT1, KMT4
DOT1-like histone H3K79 methyltransferase
GO Process (3)
GO Function (3)
GO Component (0)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Homo sapiens
PREY
PSMA4
HC9, HsT17706, PSC9
proteasome (prosome, macropain) subunit, alpha type, 4
GO Process (21)
GO Function (1)
GO Component (10)
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
Combinatorial targeting of a chromatin complex comprising Dot1L, menin and the tyrosine kinase BAZ1B reveals a new therapeutic vulnerability of endocrine therapy-resistant breast cancer.
Targeting vulnerabilities of cancer cells by inhibiting key regulators of cell proliferation or survival represents a promising way to overcome resistance to current therapies. In breast cancer (BC), resistance to endocrine therapy results from constitutively active or aberrant estrogen receptor alpha (ER?) signaling to the genome. Targeting components of the ER? pathway in these tumors represents, therefore, a rational way ... [more]
Breast Cancer Res Dec. 18, 2021; 24(1);52 [Pubmed: 35850772]
Throughput
- Low Throughput
Curated By
- BioGRID