BAIT
CCDC8
3M3, PPP1R20, p90
coiled-coil domain containing 8
GO Process (3)
GO Function (0)
GO Component (4)
Gene Ontology Biological Process
Gene Ontology Cellular Component
Homo sapiens
PREY
RAB14
FBP, RAB-14, RP11-165P4.4
RAB14, member RAS oncogene family
GO Process (12)
GO Function (5)
GO Component (19)
Gene Ontology Biological Process
- GTP catabolic process [IDA]
- Golgi to endosome transport [ISS, TAS]
- Rab protein signal transduction [IBA]
- embryo development [ISS]
- endocytic recycling [IDA]
- fibroblast growth factor receptor signaling pathway [ISS]
- intracellular protein transport [IBA]
- intracellular transport [NAS]
- membrane organization [TAS]
- phagolysosome assembly involved in apoptotic cell clearance [IBA]
- regulation of protein localization [IDA]
- vesicle-mediated transport [NAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- Golgi apparatus [IBA]
- Golgi stack [ISS]
- cytoplasmic vesicle membrane [TAS]
- cytosol [ISS]
- early endosome [IBA, ISS]
- extracellular vesicular exosome [IDA]
- intracellular [IDA]
- intracellular membrane-bounded organelle [IDA]
- late endosome [ISS]
- lysosomal membrane [IDA]
- lysosome [ISS]
- nuclear outer membrane-endoplasmic reticulum membrane network [ISS]
- perinuclear region of cytoplasm [ISS]
- phagocytic vesicle [IDA]
- plasma membrane [ISS]
- primary cilium [IDA]
- recycling endosome [IDA]
- rough endoplasmic reticulum [ISS]
- trans-Golgi network transport vesicle [ISS]
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