LIG4 Western Blot Kit
- Known as:
- LIG4 Western Blot Kit
- Catalog number:
- ARPK34122_T100
- Product Quantity:
- 25 Western Blots
- Category:
- -
- Supplier:
- ACR
- Gene target:
- LIG4 Western Blot Kit
Related genes to: LIG4 Western Blot Kit
- Gene:
- LIG4 NIH gene
- Name:
- DNA ligase 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-10
- Date modifiied:
- 2019-04-23
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- Chromosomal DNA double-strand breaks (DSBs) are repaired by two fundamentally different mechanisms: homologous recombination (HR) and nonhomologous end joining (NHEJ). While NHEJ requires the Ku70-Ku80 heterodimer (Ku) and DNA ligase IV (LIG4), recent work has established a Ku/LIG4-independent mechanism for DSB joining, referred to as alternative end-joining or theta-mediated end-joining (TMEJ). Cells lacking NHEJ and TMEJ repair DSBs in a homology-dependent manner. Here we show that APOBEC3G (A3G), a cytoplasmic antiviral protein that possesses cytidine deaminase activity on ssDNA and inhibits the replication of various types of viruses such as HIV, affects DSB repair in the human lymphocyte cell line Nalm-6. We observed that genetic deletion of A3G in LIG4-null cells resulted in (a) reduced sensitivity to replication-dependent as well as -independent DSBs, (b) enhanced frequency of HR in chromosomal and extrachromosomal reporter assays, and (c) increased frequency of TMEJ-dependent random integration as well as HR-mediated targeted integration (gene targeting). Our results suggest that human A3G, albeit mainly cytoplasmic, acts to suppress HR and TMEJ during DSB repair, particularly when NHEJ is compromised. - Source: PubMed
Publication date: 2026/07/06
Saito ShintaMurayama MioriArai UsakiAkatsu SekifumiYamamoto AmiKadoguchi MisakiAdachi Noritaka - Premature ovarian insufficiency (POI) is a heterogeneous reproductive disorder, with genetic factors, particularly defects in DNA damage response pathways, increasingly implicated in its pathogenesis. DNA ligase IV (LIG4) is a key enzyme in the non-homologous end joining (NHEJ) pathway responsible for repairing DNA double-strand breaks (DSBs). However, its role in non-syndromic POI remains unclear. This study aimed to investigate the potential contribution of LIG4 variants to non-syndromic POI. - Source: PubMed
Publication date: 2026/06/24
Yu ShaZhou XingyuLai YunhuiTang ShuyanChen Shiling - The DNA damage response (DDR) is a complex network of cellular pathways that ensures the faithful maintenance of our genomes upon a wide array of genomic insults. To elucidate the functional architecture of this network, we conducted unbiased genetic interaction screens using the Cas12a genome editor to disrupt 233 DDR genes frequently mutated in cancer and other genetic diseases, either individually or in pairwise combinations. This approach enabled us to assess the phenotypic effects induced by the disruption of >27,000 DDR gene pair combinations under unperturbed cell growth conditions. From this analysis, we identified over 750 high-confidence positive (buffering) or negative (synthetic lethal/sick) gene-gene interactions, along with multiple connections between previously unlinked DDR pathways and modules, allowing us to define novel aspects of the cellular response to spontaneous, DNA replication-associated DNA damage. Among the identified genetic interactions, we uncovered profound synthetic lethal interactions between genes encoding 1) the translesion polymerase REV1-Pol ζ complex and the MCM8-MCM9-HROB DNA helicase complex; 2) Fanconi Anemia (FA) proteins and the mitotic DNA repair factors GEN1, CIP2A, and RHINO; and 3) the DNA translocase SMARCAL1 and components of the FANCM complex, suggesting novel opportunities for targeted therapies in tumors carrying mutations in these genes. Additionally, we identified robust suppressor interactions between the gene encoding the nuclease APOLLO and the core non-homologous end joining (NHEJ) genes , , and , suggesting that NHEJ impairs the fitness of APOLLO-deficient cells. This work provides a functional map of the DDR network and demonstrates the power of Cas12a-based screens for identifying synthetic lethal and buffering interactions with therapeutic potential. - Source: PubMed
Publication date: 2026/06/08
Hayward Samuel BVaitsiankova AlinaLama-Diaz TomasChou JuihsuanTaglialatela AngeloHuang Jen-WeiWijesekarahanthi YodharaudshaniHeyza Joshua RLeuzzi GiuseppeChen ChuanyuanWong NancyLhakhang TenzinFu XiBuendia Alejandro LGheorghe VeronicaAnvar Nazanin EsmaeiliSchmidt Jens CNussenzweig AndreRabadan RaulCostanzo VincenzoGuérois RaphaëlHart TraverCiccia Alberto - Severe combined immune deficiency (SCID) is a rare inherited defect of lymphocytes causing life-threatening opportunistic infections in early infancy. Data on SCID from China are limited. This study explores the clinical, immunologic, and genetic features of a SCID cohort from Yunnan Province in China and reports novel variants. We collated clinical, laboratory, and molecular details from patients with a clinical profile suggestive of SCID. Trio-based whole-exome sequencing was performed to identify genetic variants. For the 9 previously reported variants identified in our cohort, we systematically reviewed the literature for additional cases carrying the same variants and compared clinical and immunologic features. Eleven infant patients (8 males and 3 females) were included. Molecular diagnoses were obtained in 10 patients, as follows: IL2RG (3), RAG2 (3), LIG4 (2), DCLRE1C (1), and CD3D (1). Nine patients presented with classic SCID features within the first 3 months of life. Eleven variants were identified: 2 novel RAG2 variants (p.L469P and p.Q492R) and 9 variants previously reported in SCID-associated genes. One patient with the p.Q492R variant exhibited a relatively milder clinical course. An extremely rare case of Omenn syndrome due to IL2RG deficiency was also observed. Ten of 11 patients died within 6 months of age. The literature review identified 94 additional cases carrying these same variants; clinical presentations were generally consistent with our patients, although some variability was observed. We characterized the clinical and genetic profiles of 11 SCID patients from Yunnan, China, identifying two novel RAG2 variants. While these findings expand the mutational spectrum in understudied populations, the high mortality and diagnostic delays observed here underscore the critical need for universal newborn screening in China. Further functional studies are required to confirm the impact of the identified variants. - Source: PubMed
Publication date: 2026/05/28
Wang YanjunJin RuohongHan QianHang LingLv LingChen GuizhiHu RongXiao Shufang - The development of engineered Chinese Hamster Ovary (CHO) cell lines capable of long-term, stable, and efficient recombinant protein expression is essential for industrial biologics manufacturing. Traditional random integration is hindered by epigenetic silencing and position effects, while current site-specific strategies are restricted by a limited stable library. To address this, we established a screening strategy based on two core criteria for ideal loci: 1) the capacity for sustained exogenous protein expression and 2) minimal impact on host cell physiology. By analyzing chromosomal location and expression data from 52 known stable loci, we identified 3,152 highly expressed genes. Subsequent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses excluded genes essential for core growth and metabolism, yielding 252 candidate sites. These were further refined to 25 ideal candidate loci by evaluating their betweenness centrality in a protein-protein interaction (PPI) network, prioritizing hubs with potential genomic stability. After 40 generations of continuous culture, the Enhanced Green Fluorescent Protein (EGFP)-positive rates of DNA ligase 4-like protein (LIG4), L-threonine 3-dehydrogenase, mitochondrial (LOC100759874), and alpha-aminoadipic semialdehyde synthase, mitochondrial (AASS), remained above 95%. This study established an orthogonal functional enrichment screening strategy, which significantly improved the discovery efficiency of stable expression sites in CHO cells and laid a foundation for constructing highly stable recombinant cell lines suitable for industrial production. - Source: PubMed
Publication date: 2026/05/26
Liu YazhouDing XuefengMou LuLi XuerouCai YanfeiZhang LinpeiJin JianChen Yun