BAIT
CLEC16A
Gop-1, KIAA0350
C-type lectin domain family 16, member A
GO Process (0)
GO Function (0)
GO Component (0)
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
CLEC16A interacts with retromer and TRIM27, and its loss impairs endosomal trafficking and neurodevelopment.
CLEC16A is a membrane-associated C-type lectin protein that functions as a E3-ubiquitin ligase. CLEC16A regulates autophagy and mitophagy, and reportedly localizes to late endosomes. GWAS studies have associated CLEC16A SNPs to various auto-immune and neurological disorders, including multiple sclerosis and Parkinson disease. Studies in mouse models imply a role for CLEC16A in neurodegeneration. We identified bi-allelic CLEC16A truncating variants in ... [more]
Hum Genet Mar. 01, 2023; 142(3);379-397 [Pubmed: 36538041]
Throughput
- Low Throughput
Curated By
- BioGRID