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
MIF
GIF, GLIF, MMIF
macrophage migration inhibitory factor (glycosylation-inhibiting factor)
GO Process (21)
GO Function (7)
GO Component (6)
Gene Ontology Biological Process
- carboxylic acid metabolic process [IDA]
- cell proliferation [IDA]
- cell surface receptor signaling pathway [IDA]
- negative regulation of DNA damage response, signal transduction by p53 class mediator [IDA]
- negative regulation of apoptotic process [IDA]
- negative regulation of cell aging [IDA]
- negative regulation of cell cycle arrest [IDA]
- negative regulation of gene expression [IDA]
- negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator [IDA]
- positive chemotaxis [IDA]
- positive regulation of B cell proliferation [IDA]
- positive regulation of ERK1 and ERK2 cascade [IDA]
- positive regulation of cytokine secretion [IDA]
- positive regulation of fibroblast proliferation [IDA]
- positive regulation of peptidyl-serine phosphorylation [IDA]
- positive regulation of peptidyl-tyrosine phosphorylation [IDA]
- positive regulation of phosphorylation [IDA]
- positive regulation of protein kinase A signaling [IDA]
- prostaglandin biosynthetic process [IDA]
- protein homotrimerization [IPI]
- regulation of macrophage activation [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
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