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Human Polyclonal LIG4 Primary Antibody for IHC (p), IHC - ABIN189697
Ducu, Dayaram, Marriott: The HTLV-1 Tax oncoprotein represses Ku80 gene expression. in Virology 2011
Show all 2 Pubmed References
Human Polyclonal LIG4 Primary Antibody for ICC, IF - ABIN4305497
Sousa, Zub, Aas, Hanssen-Bauer, Demirovic, Sarno, Tian, Liabakk, Slupphaug: An inverse switch in DNA base excision and strand break repair contributes to melphalan resistance in multiple myeloma cells. in PLoS ONE 2013
DNA ligase IV (LIG4) is not essential for telomere joining.
This study shown that both ligase IV and XRCC4 (show XRCC4 Antibodies) may act in concert to modulate the development of glioma.
We demonstrated an association between six previously published single nucleotide polymorphisms (rs15869 [ BRCA2 (show BRCA2 Antibodies)], rs1805389 [ LIG4], rs8079544 [ TP53 (show TP53 Antibodies)], rs25489 [ XRCC1 (show XRCC1 Antibodies)], rs1673041 [ POLD1 (show POLD1 Antibodies)], and rs11615 [ ERCC1 (show ERCC1 Antibodies)]) and subsequent CNS tumors in survivors of childhood cancer treated by radiation therapy.
In a recombinant PNKP (show PNKP Antibodies)-XRCC4 (show XRCC4 Antibodies)-LigIV complex, both the PNKP (show PNKP Antibodies) FHA (show CRY2 Antibodies) and catalytic domains contact the XRCC4 (show XRCC4 Antibodies) coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP (show PNKP Antibodies) and XRCC4 (show XRCC4 Antibodies)-LigIV regulate PNKP (show PNKP Antibodies) recruitment and activity within NHEJ.
Data suggest that stimulation of Artemis nuclease/DCLRE1C (show DCLRE1C Antibodies) activity by XRCC4 (show XRCC4 Antibodies)-DNA ligase IV hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 (show XRCC4 Antibodies) = X-ray repair cross complementing 4)
found that the rs228593, rs2267437 and rs1805388 functional polymorphisms probably alter the level of expression of the ATM (show ATM Antibodies), XRCC6 (show XRCC6 Antibodies) and LIG4 genes, respectively, being important in the maintenance of genomic instability in MDS (show PAFAH1B1 Antibodies)
marked overlap of dyskeratosis congenita with four other genetic syndromes, confounding accurate diagnosis and subsequent management. Patients with clinical features of dyskeratosis congenita need to have genetic analysis of USB1 (show USB1 Antibodies), LIG4 and GRHL2 (show GRHL2 Antibodies) in addition to the classical dyskeratosis congenita genes and telomere length measurements.
The rs1805388 in LIG4 was associated with increased radioresistance.
LIG4 is highly upregulated in human colorectal cancer cells.
Five novel mutations in LIG4 and a potential hotspot mutation (c.833G > T; p.R278L) in the Chinese population with LIG4 deficiency syndrome were identified.
Our study identifies LIG4 as a predictor of an increased risk for early biochemical recurrence in prostate cancer
The data firmly demonstrate Lig4(R278H) activity renders nonhomologous end-joining (NHEJ) DNA repair to be more error-prone, and predict increased error-prone NHEJ and A-EJ suppression as the cause of defective B lymphopoiesis in Lig4 patients.
To promote homology-directed r at the expense of nonhomologous end joining , we targeted DNA ligase IV, a key enzyme in the NHEJ pathway, using the inhibitor Scr7. This approach should be applicable to other customizable endonucleases
Lig4 and XRCC1 (show XRCC1 Antibodies) double-deficient cells switch as efficiently as Lig4-deficient cells, clearly indicating that XRCC1 (show XRCC1 Antibodies) is dispensable for A-EJ in CH12F3 cells during class switch recombination
These studies provide insight into the interplay between DNA damage responses in the developing brain and the DNA ligase IV plat (show PLAT Antibodies) the role in repairing endogenously arising DNA double-strand breaks.
Lig4-deficient B cells have reduced, but still substantial, immunoglobulins class switch recombination
Homozygous DNA ligase IV R278H mutation in mice leads to leaky SCID (show PRKDC Antibodies) and represents a model for human LIG4 syndrome.
Lig4 and Rad54 (show RAD54L Antibodies) cooperate to support cellular proliferation, dna repair, and prevent chromosome and single chromatid aberrations
LIG4 mutations can result in either a developmental defect with immunological abnormalities or a severe combined immunodeficiency (show PRKDC Antibodies) picture with normal development.
DNA Ligase IV is engaged in extrachromosomal circular major satellite DNA synthesis
DNA-PK kinase activity results in disassembly of the Ku/DNA ligase IV/Xrcc4 (show XRCC4 Antibodies) complex
The protein encoded by this gene is a DNA ligase that joins single-strand breaks in a double-stranded polydeoxynucleotide in an ATP-dependent reaction. This protein is essential for V(D)J recombination and DNA double-strand break (DSB) repair through nonhomologous end joining (NHEJ). This protein forms a complex with the X-ray repair cross complementing protein 4 (XRCC4), and further interacts with the DNA-dependent protein kinase (DNA-PK). Both XRCC4 and DNA-PK are known to be required for NHEJ. The crystal structure of the complex formed by this protein and XRCC4 has been resolved. Defects in this gene are the cause of LIG4 syndrome. Alternatively spliced transcript variants encoding the same protein have been observed.
DNA ligase 4
, ligase IV, DNA, ATP-dependent
, DNA ligase IV
, DNA ligase (ATP) 4
, ligase4-like protein
, DNA ligase 4-like
, dsDNA break repair ligase
, polydeoxyribonucleotide synthase [ATP] 4
, DNA joinase
, DNA repair enzyme
, polynucleotide ligase