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
ARHGEF2
GEF, GEF-H1, GEFH1, LFP40, P40, RP11-336K24.3
Rho/Rac guanine nucleotide exchange factor (GEF) 2
GO Process (24)
GO Function (8)
GO Component (8)
Gene Ontology Biological Process
- actin filament organization [IMP]
- apoptotic signaling pathway [TAS]
- cell morphogenesis [IMP]
- cellular hyperosmotic response [ISS]
- cellular response to muramyl dipeptide [IDA]
- cellular response to tumor necrosis factor [ISS]
- intracellular protein transport [NAS]
- negative regulation of extrinsic apoptotic signaling pathway via death domain receptors [ISS]
- negative regulation of intrinsic apoptotic signaling pathway in response to osmotic stress [ISS]
- negative regulation of microtubule depolymerization [IMP]
- negative regulation of necroptotic process [ISS]
- neurotrophin TRK receptor signaling pathway [TAS]
- positive regulation of NF-kappaB transcription factor activity [IDA]
- positive regulation of Rac GTPase activity [IDA]
- positive regulation of Rho GTPase activity [IDA]
- positive regulation of apoptotic process [TAS]
- positive regulation of interleukin-6 production [IDA]
- positive regulation of peptidyl-tyrosine phosphorylation [IDA]
- positive regulation of transcription from RNA polymerase II promoter [IDA]
- positive regulation of tumor necrosis factor production [IDA]
- regulation of Rho protein signal transduction [NAS]
- regulation of cell proliferation [TAS]
- regulation of small GTPase mediated signal transduction [TAS]
- small GTPase mediated signal transduction [TAS]
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