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The protein encoded by RECQL4 is a DNA helicase that belongs to the RecQ helicase family. Additionally we are shipping RECQL4 Antibodies (37) and RECQL4 Proteins (3) and many more products for this protein.
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RecQ4 plays an important role in the conversion of pre-initiation complexes into active replisomes requiring the unwinding of origin DNA in vertebrates.
RecQL4 is loaded adjacent to Ku heterodimer-binding sites on damaged chromatin, and functions in the repair of double-stranded DNA breaks.
RecQ4 performs an essential role in the assembly of replication machinery through interaction with Cut5 (show TOPBP1 ELISA Kits) in vertebrates.
RECQL4 is tumour promoting in established breast cancers
RecQL4-dependent association of Mcm10 (show MCM10 ELISA Kits) and Ctf4 (show WDHD1 ELISA Kits) with replication origins appears to be the first important step controlled by S phase promoting kinases and checkpoint pathways for the initiation of DNA replication in human cells.
No RECQL4 mutations were found in the BGS group without poikiloderma, confirming that RECQL4 sequencing was not indicated in this phenotype.
This finding provided the key to unravel the correlation between the RECQL4 genotype and the mild phenotype of the two siblings of Rothmund-Thomson Syndrome.
The N-terminus of human RecQL4 acts as a complex moderator of DNA transactions that are mediated by multiple DNA-binding sites.
RECQL4 stimulates higher order DNA binding of Ku70 (show XRCC6 ELISA Kits)/Ku80 (show XRCC5 ELISA Kits) to a blunt end DNA substrate. Taken together, these results implicate that RECQL4 participates in the NHEJ pathway of DSB repair via a functional interaction with the Ku70 (show XRCC6 ELISA Kits)/Ku80 (show XRCC5 ELISA Kits) complex.
The highly cancer-prone RECQ4 ID mutant failed to interact with p32, leading to increases in mtDNA copy number and MT dysfunction.
Dysfunction of RECQL4 increases DNA damage and triggers premature senescence in both human and mouse cells, which may contribute to symptoms in Rothmund-Thompson syndrome patients.
Elevated expression of RECQL4 accompanies progression of the Rothmund-Thomson Syndrome into osteosarcoma in humans and mice.
Molecular analyses show the presence of a novel truncating mutation and of a known missense mutation, p.R1021W, located outside of the helicase domain, which has been found in several patients either in a compound heterozygous state or alone.
RECQL4 is essential for normal bone development. Animals with no Recql4 in bone cells did not develop osteosarcoma.
findings show that RECQL4 is critical for skeletal development by modulating p53 (show TP53 ELISA Kits) activity in vivo.
data indicate that RECQL4 participates in DNA replication rather than genome stability and identify RECQL4 as a regulator of hematopoiesis with a nonredundant role compared with other RecQ helicases
dysfunction of RECQL4 increases DNA damage and triggers premature senescence in both human and mouse cells, which may contribute to Rothmund-Thomson syndrome features in mice.
Recql4-deficient mice show growth retardation and skin abnormalities.
Recql4 functions as a regulatory protein during osteoprogenitor proliferation, a critical cellular event during skeleton development.
we define a small core bidirectional promoter that drives expression of the mouse genes Recql4, on one strand, and Lrrc14 (show LRRC14 ELISA Kits); a novel member of the LRR gene family, on the opposite strand
The protein encoded by this gene is a DNA helicase that belongs to the RecQ helicase family. DNA helicases unwind double-stranded DNA into single-stranded DNAs and may modulate chromosome segregation. This gene is predominantly expressed in thymus and testis. Mutations in this gene are associated with Rothmund-Thomson, RAPADILINO and Baller-Gerold syndromes.
ATP-dependent DNA helicase Q4
, RecQ protein-like 4
, ATP-dependent DNA helicase Q4-like
, DNA helicase, RecQ-like type 4
, DNA helicase, RecQ-like, type 4
, RecQ helicase protein-like 4