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
DDX5
G17P1, HLR1, HUMP68, p68
DEAD (Asp-Glu-Ala-Asp) box helicase 5
GO Process (11)
GO Function (7)
GO Component (7)
Gene Ontology Biological Process
- cell growth [NAS]
- intrinsic apoptotic signaling pathway by p53 class mediator [IMP]
- mRNA splicing, via spliceosome [IC]
- negative regulation of transcription from RNA polymerase II promoter [IDA]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- positive regulation of intracellular estrogen receptor signaling pathway [IDA]
- positive regulation of transcription from RNA polymerase II promoter [IDA]
- regulation of alternative mRNA splicing, via spliceosome [IDA]
- regulation of androgen receptor signaling pathway [IMP]
- regulation of osteoblast differentiation [ISS]
- regulation of skeletal muscle cell differentiation [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