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Human Polyclonal LIG4 Primary Antibody für 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 für 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 (zeige XRCC4 Antikörper) may act in concert to modulate the development of glioma.
We demonstrated an association between six previously published single nucleotide polymorphisms (rs15869 [ BRCA2 (zeige BRCA2 Antikörper)], rs1805389 [ LIG4], rs8079544 [ TP53 (zeige TP53 Antikörper)], rs25489 [ XRCC1 (zeige XRCC1 Antikörper)], rs1673041 [ POLD1 (zeige POLD1 Antikörper)], and rs11615 [ ERCC1 (zeige ERCC1 Antikörper)]) and subsequent CNS tumors in survivors of childhood cancer treated by radiation therapy.
In a recombinant PNKP (zeige PNKP Antikörper)-XRCC4 (zeige XRCC4 Antikörper)-LigIV complex, both the PNKP (zeige PNKP Antikörper) FHA (zeige CRY2 Antikörper) and catalytic domains contact the XRCC4 (zeige XRCC4 Antikörper) coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP (zeige PNKP Antikörper) and XRCC4 (zeige XRCC4 Antikörper)-LigIV regulate PNKP (zeige PNKP Antikörper) recruitment and activity within NHEJ.
Data suggest that stimulation of Artemis nuclease/DCLRE1C (zeige DCLRE1C Antikörper) activity by XRCC4 (zeige XRCC4 Antikörper)-DNA ligase IV hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 (zeige XRCC4 Antikörper) = X-ray repair cross complementing 4)
found that the rs228593, rs2267437 and rs1805388 functional polymorphisms probably alter the level of expression of the ATM (zeige ATM Antikörper), XRCC6 (zeige XRCC6 Antikörper) and LIG4 genes, respectively, being important in the maintenance of genomic instability in MDS (zeige PAFAH1B1 Antikörper)
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 (zeige USB1 Antikörper), LIG4 and GRHL2 (zeige GRHL2 Antikörper) 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 (zeige XRCC1 Antikörper) double-deficient cells switch as efficiently as Lig4-deficient cells, clearly indicating that XRCC1 (zeige XRCC1 Antikörper) 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 (zeige PLAT Antikörper) 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 (zeige PRKDC Antikörper) and represents a model for human LIG4 syndrome.
Lig4 and Rad54 (zeige RAD54L Antikörper) 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 (zeige PRKDC Antikörper) 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 (zeige XRCC4 Antikörper) 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