BAIT
OBSL1
obscurin-like 1
GO Process (7)
GO Function (2)
GO Component (8)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
C1QBP
GC1QBP, HABP1, SF2p32, gC1Q-R, gC1qR, p32
complement component 1, q subcomponent binding protein
GO Process (21)
GO Function (9)
GO Component (7)
Gene Ontology Biological Process
- blood coagulation [TAS]
- blood coagulation, intrinsic pathway [TAS]
- immune response [TAS]
- mature ribosome assembly [IMP]
- negative regulation of MDA-5 signaling pathway [IDA]
- negative regulation of RIG-I signaling pathway [IDA]
- negative regulation of defense response to virus [IMP]
- negative regulation of interferon-gamma production [IDA]
- negative regulation of interleukin-12 production [IDA]
- negative regulation of mRNA splicing, via spliceosome [IDA]
- negative regulation of transcription from RNA polymerase II promoter [IDA]
- phosphatidylinositol 3-kinase signaling [IMP]
- positive regulation of apoptotic process [IMP]
- positive regulation of cell adhesion [IMP]
- positive regulation of dendritic cell chemotaxis [IMP]
- positive regulation of mitochondrial translation [ISS]
- positive regulation of neutrophil chemotaxis [IDA]
- positive regulation of protein kinase B signaling [IMP]
- positive regulation of substrate adhesion-dependent cell spreading [IMP]
- positive regulation of trophoblast cell migration [IMP]
- regulation of complement activation [IDA]
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
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