Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Mouse (Murine) Antibodies:
anti-Rat (Rattus) Antibodies:
Go to our pre-filtered search.
Human Polyclonal LIG4 Primary Antibody for IHC, WB - ABIN6673104
Li, Zhang, Chen, Guo, Zhang, Tang, Xu, Zhang, Tao, Wang, Jiang, Sun, Mao: Impaired DNA double-strand break repair contributes to the age-associated rise of genomic instability in humans. in Cell death and differentiation 2017
Show all 2 Pubmed References
Mouse (Murine) Polyclonal LIG4 Primary Antibody for IHC, WB - ABIN3022475
Zhang, Chang, Sun, Chen, Yang, Tang, Jing, Kang, He, Wu, Wei, Wang, Xu, Zhu, Shen, Zeng, Wang, Liu, Zhang, Mao, Jiang, Sun: Histone H3K27 methylation modulates the dynamics of FANCD2 on chromatin to facilitate NHEJ and genome stability. in Journal of cell science 2018
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.
Cells doubly deficient in Pol theta; and Lig4 exhibit 100% gene-targeting efficiency because of virtually no random integration events.
These studies provide a scaffold for defining impacts of LigIV catalytic core mutations and deficiencies in human LIG4 syndrome.
study demonstrated that there was an association between DNA ligase 4 Thr9Ile polymorphism and male infertility and suggests CT genotype as a risk factor for male infertility
An increased frequency of binucleated lymphocytes with micronuclei was increased in carriers of the T/T genotype of the LIG4 (rs1805388) gene compared to miners harbouring the C/T genotype.
Cellular NHEJ of diverse ends thus identifies the steps necessary for repair through LIG4-mediated sensing of differences in end structure and consequent dynamic remodeling of aligned ends.
This study shown that both ligase IV and XRCC4 may act in concert to modulate the development of glioma.
We demonstrated an association between six previously published single nucleotide polymorphisms (rs15869 [ BRCA2], rs1805389 [ LIG4], rs8079544 [ TP53], rs25489 [ XRCC1], rs1673041 [ POLD1], and rs11615 [ ERCC1]) and subsequent CNS tumors in survivors of childhood cancer treated by radiation therapy.
In a recombinant PNKP-XRCC4-LigIV complex, both the PNKP FHA and catalytic domains contact the XRCC4 coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP and XRCC4-LigIV regulate PNKP recruitment and activity within NHEJ.
Data suggest that stimulation of Artemis nuclease/DCLRE1C activity by XRCC4-DNA ligase IV hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 = X-ray repair cross complementing 4)
found that the rs228593, rs2267437 and rs1805388 functional polymorphisms probably alter the level of expression of the ATM, XRCC6 and LIG4 genes, respectively, being important in the maintenance of genomic instability in MDS
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, LIG4 and GRHL2 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 genetic polymorphisms in LIG4 rs1805388 and HSPB1 rs2868371 were not obviously correlated with the risk of radiation pneumonitis and radiation-induced lung injury of lung cancer.
our results suggest that LIG4 rs10131 polymorphism in the DNA repair pathways plays an important role in the risk of glioma in a Chinese population.
Our data showed that Cd altered the phosphorylation of DNA-PKcs, and reduced the expression of both XRCC4 and Ligase IV in irradiated cells.
despite several limitations, this meta-analysis suggested that LIG4 T9I genetic variant is associated with a decreased risk of cancer among Caucasians, however, the rs1805386 gene polymorphism is not a risk factor of cancer.
High LIG4 expression is associated with less radiosensitivity of nasopharyngeal 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 double-deficient cells switch as efficiently as Lig4-deficient cells, clearly indicating that XRCC1 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 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 and represents a model for human LIG4 syndrome.
Lig4 and Rad54 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 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 complex
Results describe the activity requirements for DNA ligases III and IV in the pathways of non-homologous DNA end joining.
Data show that disruption of the DNA ligase IV gene in a B cell line severely inhibits the initial rate of class switch recombination and causes a late cell proliferation defect under cytokine stimulation.
particular features of the c-Myc locus select it as a preferential translocation/amplification target, compared to the endogenous N-myc locus, in Lig4/p53-deficient pro-B cell lymphomas
the Lig4Y288C mutation leads to multiple defects in lymphocyte development and function, including impaired V(D)J recombination, peripheral lymphocyte survival and proliferation, and B cell class switch recombination
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