G22P1 antibody - N-terminal region (ARP34116_T100)
- Known as:
- G22P1 (anti-) - N-terminal region (ARP34116_T100)
- Catalog number:
- arp34116_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- G22P1 antibody - N-terminal region (ARP34116_T100)
Related genes to: G22P1 antibody - N-terminal region (ARP34116_T100)
- 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 antibody - N-terminal region (ARP34116_T100)
Related articles to: G22P1 antibody - N-terminal region (ARP34116_T100)
- 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 - 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 - Loss of histone deacetylase 5 (HDAC5) is frequently observed in multiple malignancies, including pancreatic ductal adenocarcinoma (PDAC), and is associated with poor patient survival. Although HDAC5 has been implicated in DNA damage repair, the molecular mechanisms by which it regulates DNA double-strand break (DSB) repair pathway choice remain unclear. Using PDAC cell lines, genetically engineered mouse models, patient-derived organoids, and biochemical assays, we investigated the role of HDAC5 in DNA end resection and homologous recombination (HR). Protein interactions, post-translational modifications, DNA repair pathway activity, and cellular responses to DNA damage and PARP inhibition were systematically analyzed. We identify HDAC5 as a critical regulator of DNA end resection and HR through deacetylation of Ku70. DNA damage induces casein kinase 2 (CK2)-mediated phosphorylation of HDAC5, promoting its nuclear translocation. Nuclear HDAC5 directly deacetylates Ku70 at lysine 287, facilitating Ku70 dissociation from DSB sites, thereby enabling DNA end resection and HR repair. In contrast, HDAC5 loss or CK2 inhibition results in Ku70 K287 hyperacetylation, prolonged retention of the Ku heterodimer at DSBs, impaired DNA end resection, and suppression of HR. Consequently, HDAC5-deficient PDAC cells exhibit increased sensitivity to PARP inhibitors, while pharmacological CK2 inhibition sensitizes HDAC5-proficient tumors to PARP inhibition. These findings uncover a previously unrecognized CK2-HDAC5-Ku70 signaling axis that governs DNA repair pathway choice by regulating DNA end resection. Targeting this axis provides a mechanistic rationale for enhancing PARP inhibitor sensitivity in PDAC, including tumors without classical homologous recombination deficiency. - Source: PubMed
Publication date: 2026/01/08
Liang XueyiZhao JingyuanLi ShoukangWei RuozhengYu HaixinZhang QiyueFu QixunQin GengduZhao YuhanLiu JiayingLiu ZhiqiangPeng TaoMeng JunpengGou ShanmiaoYin TaoWu HeshuiWang BoZhou Yingke