BAIT
MCPH1
BRIT1, MCT
microcephalin 1
GO Process (1)
GO Function (2)
GO Component (1)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
DNAJA3
HCA57, TID1, hTID-1
DnaJ (Hsp40) homolog, subfamily A, member 3
GO Process (18)
GO Function (7)
GO Component (13)
Gene Ontology Biological Process
- activation of cysteine-type endopeptidase activity involved in apoptotic process [IDA]
- mitochondrion organization [IBA]
- negative regulation of I-kappaB kinase/NF-kappaB signaling [IDA]
- negative regulation of NF-kappaB transcription factor activity [IDA]
- negative regulation of apoptotic process [IDA]
- negative regulation of cell proliferation [IDA]
- negative regulation of cysteine-type endopeptidase activity involved in apoptotic process [IDA]
- negative regulation of interferon-gamma-mediated signaling pathway [IDA]
- negative regulation of protein kinase activity [IDA]
- negative regulation of transcription from RNA polymerase II promoter [IDA]
- neuromuscular junction development [IDA]
- positive regulation of apoptotic process [IDA]
- positive regulation of protein ubiquitination [IDA]
- protein folding [IDA]
- protein refolding [IBA]
- protein stabilization [IDA]
- response to interferon-gamma [IDA]
- skeletal muscle acetylcholine-gated channel clustering [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- I-kappaB/NF-kappaB complex [IDA]
- IkappaB kinase complex [IDA]
- actin filament [IDA]
- cytoplasm [IDA]
- cytosol [IMP]
- extrinsic component of plasma membrane [ISS]
- intracellular membrane-bounded organelle [IDA]
- mitochondrial matrix [IDA]
- mitochondrial nucleoid [IDA]
- mitochondrion [IDA]
- neuromuscular junction [ISS]
- nucleus [IDA]
- postsynaptic membrane [ISS]
Homo sapiens
Two-hybrid
Bait protein expressed as a DNA binding domain (DBD) fusion and prey expressed as a transcriptional activation domain (TAD) fusion and interaction measured by reporter gene activation.
Publication
The E3 ubiquitin ligase APC/CCdh1 degrades MCPH1 after MCPH1-βTrCP2-Cdc25A-mediated mitotic entry to ensure neurogenesis.
Mutations of microcephalin (MCPH1) can cause the neurodevelopmental disorder primary microcephaly type 1. We previously showed that MCPH1 deletion in neural stem cells results in early mitotic entry that distracts cell division mode, leading to exhaustion of the progenitor pool. Here, we show that MCPH1 interacts with and promotes the E3 ligase βTrCP2 to degrade Cdc25A independent of DNA damage. ... [more]
EMBO J. Dec. 15, 2016; 36(24);3666-3681 [Pubmed: 29150431]
Throughput
- High Throughput
Curated By
- BioGRID