Rad51 mAb (Rad51 3C10)
- Known as:
- Rad51 mAb (Rad51 3C10)
- Catalog number:
- ASAKAM-CC260F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Rad51 mAb (Rad51 3C10)
Related genes to: Rad51 mAb (Rad51 3C10)
- Gene:
- RAD51 NIH gene
- Name:
- RAD51 recombinase
- Previous symbol:
- RAD51A, RECA
- Synonyms:
- HsRad51, HsT16930, BRCC5, FANCR
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2017-05-02
Related products to: Rad51 mAb (Rad51 3C10)
11A5 Anti-Prolyl 4-Hydroxylated FGA mAb13 X Anti INT HIV mAb14-3-3β, 30kD, Clone: 4E1, Mab anti-Mouse, Rat; WB/IP14-3-3β/ε/ζ, ~30kD, Clone: 3C8, Mab anti-Human, Mouse, Rat; WB14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC14_3_3 beta mAb;mouse, rat (4E1)14_3_3 beta_epsilon_zeta mAb;human, mouse, rat (3C8)14_3_3 beta_zeta mAb (22_ii_D8B);h, mouse, rat, bovine, canin14_3_3 beta_zeta mAb (22_ii_D8B);h, mouse, rat, bovine, canin14_3_3, Mab anti_; Clone 6A1015K allergen of House Dust Mite Dermatophagoides, Mab anti-15K allergen of House Dust Mite Dermatophagoides, Mab anti_17-Beta-Estradiol, Mab anti-; Clone: 4S42, ELISA17-estradiol, Mab anti- Related articles to: Rad51 mAb (Rad51 3C10)
- Chemoresistance remains a critical barrier to the efficacy of oxaliplatin in colon cancer treatment. While the deubiquitinating enzyme USP46 is implicated in multiple tumor progression pathways, its specific role in oxaliplatin resistance remains undetermined. Our analysis reveals that USP46 is significantly overexpressed in colon cancer tissues, with its elevated expression correlating with poor clinical outcomes in colon cancer patients. Silencing USP46 suppresses both the proliferation and metastatic potential of colon cancer cells while simultaneously enhancing cellular sensitivity to the DNA-damaging agent oxaliplatin. Mechanistically, overexpression of USP46 leads to upregulation of nuclear RAD51 expression and facilitates the assembly of RAD51 foci, thereby increasing homologous recombination repair (HRR) capacity and contributing to oxaliplatin resistance in colon cancer cells. MCM7 is identified as a bona fide substrate of USP46 by LC-MS/MS profiling. Subsequent experiments confirm that USP46 specifically removes K48-linked polyubiquitin chains from MCM7, thereby stabilizing its protein expression. Rescue assays validate that USP46 modulates RAD51 expression and HRR function in an MCM7-dependent manner. Collectively, our study uncovers a novel USP46-MCM7-RAD51 signaling cascade that confers oxaliplatin resistance in colon cancer via augmentation of HRR-dependent DNA repair, thereby establishing this axis as a promising therapeutic target for overcoming oxaliplatin resistance. - Source: PubMed
Publication date: 2026/06/25
Wu ChangleiZhu WenjieZhu ZhengmingZuo ChengXiao TaifuLiu Zitao - Head and neck squamous cell carcinoma (HNSCC) remains a highly aggressive malignancy with poor clinical outcomes. Although poly(ADP-ribose) polymerase (PARP) inhibitors have shown promising activity in tumors with homologous recombination deficiency, their efficacy in BRCA wild-type HNSCC remains limited. Reactive oxygen species (ROS)-induced DNA damage may increase cellular dependence on DNA repair pathways and thereby enhance sensitivity to PARP inhibition. This study investigated whether ROS-mediated DNA damage could sensitize BRCA wild-type HNSCC cells to the PARP inhibitor olaparib. - Source: PubMed
Publication date: 2026/07/05
Taghavi Pourianazar Negar - Genomic instability is increased in patients with inflammatory bowel disease (IBD), yet whether it contributes directly to disease pathogenesis remains unclear. Here, we identify RADX, a structural antagonist to RAD51 and a key regulator of replication fork stability, as a critical suppressor of intestinal inflammation by limiting innate immune sensing of replication-associated DNA damage. RADX deficiency exacerbates experimental colitis, with macrophages serving as the principal mediators of this phenotype. Mechanistically, RADX competes with the DNA sensor IFI16 for binding to single-stranded DNA (ssDNA). Loss of RADX promotes ssDNA accumulation, triggering IFI16-dependent activation of NF-κB signaling and inflammasome assembly, thereby driving intestinal inflammation. Consistent with these findings, two RADX variants identified in patients with IBD associate with reduced RADX protein expression, increased DNA damage signaling, and elevated IL-1β levels. Pharmacological inhibition of RAD51 with RI-1 alleviated colitis in both wild-type and Radx-deficient mice. Together, these findings establish a mechanistic link between genome instability and intestinal inflammation, identify a RADX-IFI16 checkpoint that restrains pathogenic innate immune activation, and nominate modulation of replication stress as a therapeutic strategy for IBD. - Source: PubMed
Publication date: 2026/07/24
Xian HuifangHuang WanmingChen ZhanghuaLi LiliXiong LiyaZhu JianhengJin HaolanLi XiaotianSong LizhiChen PeiyuRen LuWang WeiFang RongliChen XixiLei WenZhang DengfengLiao WeiliangHuang YuxinLew Andrew MCui JunGong SitangHuang JunRosa Duque Jaime SZhi MinGeng LanlanZhou WenhaoZhang Yuxia - HIV-1 infection triggers multiple cellular pathways that modulate viral replication and may promote latency. Central to this process is the reverse transcription of the viral RNA into DNA and its integration into host chromatin, both processes being regulated by the cell. Emerging evidence suggests that homologous recombination (HR) proteins, especially RAD51, may influence both pre- and post-integration stages. In this study, we show that HIV-1 induces the rapid formation of RAD51 nuclear foci in a BRCA1/2-dependent manner, with RAD51 loading onto viral DNA immediately during reverse transcription. Using ChIP, imaging, and biochemical assays, we demonstrate that this process enhances viral infectivity and reverse transcription efficiency. Our findings reveal a previously unidentified cellular response that recruits repair factors to viral DNA, regulating reverse transcription and influencing viral DNA fate. This work uncovers a previously unknown role for RAD51 in modulating early HIV-1 replication, providing insights into host-virus interactions and potential therapeutic strategies. - Source: PubMed
Publication date: 2026/07/24
Lapaillerie DelphineTumiotto CamilleScoca VivianaFigueiredo SuzanneMaisch MathieuBertinetti CaroleMougel MaryleneFleury FabriceLesbats PaulDelelis OlivierDutrieux JacquesDi Nunzio FrancescaParissi Vincent - This study evaluated the effects of dietary guanidinoacetic acid (GAA) supplementation (0.06%) at different feeding phases on growth performance, carcass traits, plasma biochemistry, meat quality and hepatic transcriptomic responses in broiler chickens under heat stress exposure. - Source: PubMed
Publication date: 2026/07/23
Irawan AgungSaraswati Pramita NSaputro Wahyu SDarmawan Muhammad AAkhirini NoviPradista Luthfi ASetyono WahyuYano Aan ANugroho DianRatriyanto AdiSuprayogi Wara Ps