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
PPP2R1A
PP2A-Aalpha, PP2AAALPHA, PR65A
protein phosphatase 2, regulatory subunit A, alpha
GO Process (25)
GO Function (4)
GO Component (8)
Gene Ontology Biological Process
- G2/M transition of mitotic cell cycle [TAS]
- RNA metabolic process [TAS]
- RNA splicing [NAS]
- apoptotic process [TAS]
- ceramide metabolic process [NAS]
- chromosome segregation [IDA]
- fibroblast growth factor receptor signaling pathway [TAS]
- gene expression [TAS]
- inactivation of MAPK activity [NAS]
- mRNA metabolic process [TAS]
- mitotic cell cycle [TAS]
- mitotic nuclear envelope reassembly [TAS]
- negative regulation of cell growth [NAS]
- negative regulation of tyrosine phosphorylation of Stat3 protein [NAS]
- nuclear-transcribed mRNA catabolic process, nonsense-mediated decay [TAS]
- protein complex assembly [TAS]
- protein dephosphorylation [TAS]
- regulation of DNA replication [NAS]
- regulation of Wnt signaling pathway [NAS]
- regulation of cell adhesion [NAS]
- regulation of cell differentiation [NAS]
- regulation of growth [NAS]
- regulation of transcription, DNA-templated [NAS]
- response to organic substance [NAS]
- second-messenger-mediated signaling [NAS]
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