BAIT
TMPO
CMD1T, LAP2, LEMD4, PRO0868, TP
thymopoietin
GO Process (0)
GO Function (2)
GO Component (5)
Gene Ontology Molecular Function
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
Nuclear lamina genetic variants, including a truncated LAP2, in twins and siblings with nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) is becoming the major chronic liver disease in many countries. Its pathogenesis is multifactorial, but twin and familial studies indicate significant heritability, which is not fully explained by currently known genetic susceptibility loci. Notably, mutations in genes encoding nuclear lamina proteins, including lamins, cause lipodystrophy syndromes that include NAFLD. We hypothesized that variants in lamina-associated ... [more]
Hepatology May. 01, 2018; 67(5);1710-1725 [Pubmed: 28902428]
Throughput
- High Throughput
Curated By
- BioGRID