BAIT
CUL7
3M1, KIAA0076, dJ20C7.5
cullin 7
GO Process (13)
GO Function (1)
GO Component (10)
Gene Ontology Biological Process
- Golgi organization [ISS]
- activation of signaling protein activity involved in unfolded protein response [TAS]
- cellular protein metabolic process [TAS]
- endoplasmic reticulum unfolded protein response [TAS]
- epithelial to mesenchymal transition [IDA]
- microtubule cytoskeleton organization [IMP]
- mitotic cytokinesis [IMP]
- placenta development [IDA]
- positive regulation of dendrite morphogenesis [IGI, ISS]
- protein ubiquitination [IDA, TAS]
- proteolysis [NAS]
- regulation of mitosis [IMP]
- vasculogenesis [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
PRMT5
HRMT1L5, IBP72, JBP1, SKB1, SKB1Hs
protein arginine methyltransferase 5
GO Process (13)
GO Function (7)
GO Component (4)
Gene Ontology Biological Process
- RNA metabolic process [TAS]
- cell proliferation [TAS]
- circadian regulation of gene expression [ISS]
- endothelial cell activation [IMP]
- gene expression [TAS]
- histone H4-R3 methylation [ISS, NAS]
- ncRNA metabolic process [TAS]
- peptidyl-arginine N-methylation [IDA]
- peptidyl-arginine methylation [IMP]
- peptidyl-arginine methylation, to symmetrical-dimethyl arginine [IMP]
- regulation of mitosis [TAS]
- regulation of transcription, DNA-templated [IBA]
- spliceosomal snRNP assembly [IMP, TAS]
Gene Ontology Molecular Function
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
Identifying biological pathways that underlie primordial short stature using network analysis.
Mutations in CUL7, OBSL1 and CCDC8, leading to disordered ubiquitination, cause one of the commonest primordial growth disorders, 3-M syndrome. This condition is associated with (1) abnormal p53 function, (2) GH and/or IGF1 resistance, which may relate to failure to recycle signalling molecules, and (3) cellular IGF2 deficiency. However the exact molecular mechanisms that may link these abnormalities generating growth ... [more]
J. Mol. Endocrinol. Apr. 07, 2014; 0(0); [Pubmed: 24711643]
Throughput
- High Throughput
Curated By
- BioGRID