G22P1 Mouse Monoclonal Antibody
- Known as:
- G22P1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002547-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- G22P1 Mouse Monoclonal Antibody
Related genes to: G22P1 Mouse Monoclonal Antibody
- Gene:
- XRCC6 NIH gene
- Name:
- X-ray repair cross complementing 6
- Previous symbol:
- G22P1
- Synonyms:
- D22S731, D22S671, KU70, ML8
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-06-02
Related products to: G22P1 Mouse Monoclonal Antibody
Related articles to: G22P1 Mouse Monoclonal Antibody
- Endonuclease G (EndoG) is an evolutionarily conserved enzyme that cleaves the Mixed Lineage Leukemia breakpoint cluster region (MLLbcr) under sublethal chemotherapeutic treatment conditions, causing leukemogenic chromosomal rearrangements. While endogenous inhibitors (EndoGI) control EndoG in lower organisms, no such EndoGI has been identified in mammalian cells. Due to the structural similarity of EndoGI from Drosophila melanogaster to the C-terminus (Ct) of human Ku80, we perform immunoprecipitation, surface plasmon resonance analysis and 3D molecular modeling, revealing binding of human EndoG to Ku80-Ct putatively between amino acid 110-184. Docking modeling predicts EndoGI-like peptides clustering around residues 686-707 of Ku80. Our experimental studies provide evidence that Ku80-Ct and 28-mer peptide Ku3 reduce MLLbcr breakage after doxorubicin treatment independently of DNA-PK activity. Proximity ligation and single molecule tracking studies show that Ku3 antagonizes Ku80-EndoG association and modulates chromatin-binding of EndoG. Such MLLbcr protection blocks EndoG´s pro-tumorigenic functions without limiting cytotoxicity, pursued for co-treatments that reduce secondary leukemia, a severe side effect of chemotherapy. - Source: PubMed
Publication date: 2026/04/17
Eberle JuliaSalem AhmedHofmann MaraReisser AnjaRuiz-Blanco Yasser BAlmeida-Hernandez YasserGole BorisRall-Scharpf MelanieAngulo-Capel JessicaMonecke ThomasSanchez-Garcia ElsaGebhardt J Christof MWiesmüller Lisa - DNA damage-induced by radiotherapy is a critical factor in promoting the death of colorectal cancer cells (CRC). Although high mobility group box 1 (HMGB1) reportedly plays a vital role in tumor radioresistance by modulating DNA damage repair, the precise mechanisms remain unclear. In this study, HMGB1 knockdown markedly enhanced cell apoptosis after radiation. HMGB1 downregulation significantly inhibited DNA damage repair and reactive oxygen species (ROS)-mediated redox homeostasis after irradiation in CRC cells. Mechanistically, HMGB1 interacts with KU70 via its region spanning residues 95-163. This interaction subsequently activates the non-homologous end joining (NHEJ) pathway to facilitate DNA damage repair, ultimately leading to reduced radiation-induced cell apoptosis. KU70 silencing showed the same effect as HMGB1 depletion mediated cell apoptosis and DNA damage response both in vitro and in vivo. Additionally, HMGB1 and KU70 were overexpressed in CRC tissues. Analysis of the GEPIA database indicated that elevated levels of both genes showed a trend toward association with poor patient prognosis, although this did not reach statistical significance. The current study revealed that HMGB1 may promote DNA damage repair through KU70 and its mediated NHEJ pathway to affect apoptosis in CRC cells after irradiation. Thus, targeting the HMGB1/KU70/NHEJ axis may be a potential therapeutic target to promote the response of CRC to radiotherapy and in-depth study of the specific mechanism of this axis in CRC radioresistance will help to the develop more effective treatment strategies. - Source: PubMed
Publication date: 2026/03/24
Liu XiuxinHan YuhuiKuang RuixueSheng WenjiongZhang YanJia XinyuGao XiaoxiaoMa Yanchao - Colorectal cancer (CRC) is a major health threat with limited therapies for advanced stages. Crocetin, a natural compound from saffron, has broad anticancer potential, but its mechanisms in CRC are unclear. - Source: PubMed
Publication date: 2026/03/14
Chen ShuoSu WeijunWang KaiXu MingyueSu Binjie - Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and α-synuclein aggregation, with evidence implicating impaired DNA double-strand break (DSB) repair in disease pathogenesis. This study aimed to systematically evaluate the association between genetic polymorphisms in DSB repair pathway genes, including , , , , , , , and , and PD risk, along with corresponding mRNA expression and DNA repair capacity. A total of 123 clinically diagnosed PD patients and 492 age- and sex-matched healthy controls of Taiwanese ancestry were genotyped, and transcriptional and functional assays were performed in 52 healthy controls. Nominally significant associations with PD risk were identified for four SNPs: rs5751129 ( = 3.55 × 10⁻⁵), rs28360071 ( = 0.0181), rs2735383 ( = 0.0213) and rs17772583 ( = 0.0411). Among these, rs5751129 remained statistically significant after correction for multiple comparisons. Compared to individuals with the wild-type TT genotype, carriers of the heterozygous variant (TC) and homozygous variant (CC) genotypes exhibited increased PD risks, with odds ratios of 1.86 (95% CI, 1.09–3.17) and 13.82 (95% CI, 2.74–69.54), respectively. Cumulative analysis revealed a dose-dependent increase in PD risk with multiple high-risk genotypes ( for trend = 0.0025). Functionally, the rs5751129 CC variant was associated with reduced mRNA expression ( = 0.0001) and impaired NHEJ and DSB repair capacity ( = 0.0183). These findings suggest that genetic variants in DSB genes , , and are associated with PD susceptibility in a Taiwanese population and provide preliminary functional evidence that variants contribute to compromised DNA repair. Together, the results highlight a critical role of inherited DSB repair deficiencies in PD etiology and suggest potential avenues for personalized risk prediction and prevention. - Source: PubMed
Publication date: 2026/03/11
Chen Chao-HsuanTsai Chia-WenChang Wen-ShinLu Ming-KueiCho Der-YangBau Da-Tian - The sterol regulatory element-binding transcription factor 1 (SREBP-1) plays a crucial role in the transcriptional regulation of lipogenic response genes, thereby contributing to the development of non-alcoholic fatty liver disease (NAFLD). However, the modulation of SREBP-1 transcriptional activity remains incompletely understood. Here, we report that the transcription factor FOXN3 interacts with the KU70/KU80/SREBP-1 complex, facilitating the recruitment of SREBP-1 for the transcriptional activation of lipogenic response genes. Hepatocyte-specific knockout of FOXN3 significantly alleviates the pathological progression of NAFLD by suppressing fatty acid and cholesterol synthesis. Furthermore, phosphorylation of FOXN3 at the S83 and S85 residues disrupts the stability of the KU70/KU80/FOXN3/SREBP-1 complex, which is required for SREBP-1 transcriptional activity. This disruption consequently impedes the progression of NAFLD. Clinical investigations reveal that FOXN3, KU80, and SREBP-1 co-target the promoters of lipogenic response genes in fatty liver tissues from patients. Notably, phosphorylation levels of FOXN3 at S83 and S85 are significantly reduced in fatty liver tissues compared to normal samples. This reduction enhances the enrichment of the FOXN3/SREBP-1 complex at the promoters of lipogenic response genes during the progression of NAFLD. Our study underscores the critical role of FOXN3 in maintaining the intact KU70/KU80/FOXN3/SREBP-1 complex, which is essential for SREBP-1-mediated metabolic disorders. - Source: PubMed
Du JiangJin LeleWang SuhuiHu XinghongYu JinjinYu JingyuHuo QingyangWu NanLiu XiaotianYang YanZhang YongHuang SizhouZhou JihongZheng Song GuoZheng ChunfuZhu Xinxing