BAIT
RECQL4
RECQ4
RecQ protein-like 4
GO Process (5)
GO Function (4)
GO Component (1)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Homo sapiens
PREY
STOML2
SLP-2, HSPC108
stomatin (EPB72)-like 2
GO Process (14)
GO Function (3)
GO Component (9)
Gene Ontology Biological Process
- CD4-positive, alpha-beta T cell activation [ISS]
- T cell receptor signaling pathway [IMP]
- cellular calcium ion homeostasis [IMP]
- interleukin-2 production [ISS]
- lipid localization [ISS]
- mitochondrial ATP synthesis coupled proton transport [IMP]
- mitochondrial calcium ion transport [IMP]
- mitochondrial protein processing [ISS]
- mitochondrion organization [IMP]
- positive regulation of cardiolipin metabolic process [IMP]
- positive regulation of mitochondrial DNA replication [IMP]
- positive regulation of mitochondrial membrane potential [IMP]
- protein oligomerization [IDA]
- stress-induced mitochondrial fusion [ISS]
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
Cell cycle-dependent phosphorylation regulates RECQL4 pathway choice and ubiquitination in DNA double-strand break repair.
Pathway choice within DNA double-strand break (DSB) repair is a tightly regulated process to maintain genome integrity. RECQL4, deficient in Rothmund-Thomson Syndrome, promotes the two major DSB repair pathways, non-homologous end joining (NHEJ) and homologous recombination (HR). Here we report that RECQL4 promotes and coordinates NHEJ and HR in different cell cycle phases. RECQL4 interacts with Ku70 to promote NHEJ ... [more]
Nat Commun Dec. 11, 2016; 8(1);2039 [Pubmed: 29229926]
Throughput
- High Throughput
Curated By
- BioGRID