MRE11A Blocking Peptide
- Known as:
- MRE11A Blocking Peptide
- Catalog number:
- 33r-2193
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- MRE11A Blocking Peptide
Related genes to: MRE11A Blocking Peptide
- Gene:
- MRE11 NIH gene
- Name:
- MRE11 homolog, double strand break repair nuclease
- Previous symbol:
- MRE11A
- Synonyms:
- ATLD
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-05
- Date modifiied:
- 2019-04-23
Related products to: MRE11A Blocking Peptide
Related articles to: MRE11A Blocking Peptide
- The R2TP chaperone complex comprises two AAA+ proteins, RUVBL1 and RUVBL2, along with RPAP3 and PIH1D1. R2TP functions in concert with other chaperones, such as HSP90 and HSP70, to facilitate the assembly of macromolecular complexes integral to the regulation of cell growth and proliferation. Moreover, several adaptors interact with R2TP to impart substrate specificity. Nevertheless, the precise mechanism underlying R2TP-mediated complex assembly remains unknown. This review summarizes the current knowledge regarding R2TP's involvement in the assembly, stabilization, and activity of multiple protein complexes, including box C/D and H/ACA small nucleolar ribonucleoproteins (snoRNPs), spliceosome small nuclear ribonucleoproteins (snRNPs), Tuberous sclerosis complex, axonemal dynein arms, RNA polymerases, phosphoinositide 3-kinase-related kinases (PIKK), and the MRE11-RAD50-NBS1 (MRN) complex. Additionally, the role of R2TP in ciliogenesis, circadian rhythm regulation, and transcriptional condensate formation is discussed. Finally, the latest structural studies pertaining to R2TP and its related complexes are examined. - Source: PubMed
Publication date: 2026/06/04
Mohamed MaryamaWu RuikaiHoury Walid A - PARPi are effective therapy for BRCA1/2 mutant cancers, yet recurrent PARPi resistance frequently develops. The underlying mechanism of PARPi resistance remains largely unresolved. Here, we identify STN1, a component of the CTC1/STN1/TEN1 (CST) complex, as a modulator of PARPi resistance in BRCA2-deficient cells. RNA-seq analysis of PARPi-resistant cancer cells from BRCA2-mutated backgrounds shows largely distinct transcriptomic profiles with limited overlap, suggesting multiple routes to resistance. Notably, STN1 is consistently upregulated in resistant cells. We observe that overexpression of STN1 enhances Olaparib resistance in multiple BRCA2-deficient cell lines and alleviates DNA damage under replication stress. Mechanistically, we find that STN1 overexpression increases RAD51 loading to stalled replication forks while restricting MRE11 recruitment in BRCA2-deficient cells, thereby protecting stalled forks from nascent-strand degradation. Furthermore, STN1 overexpression rescues the accumulation of ssDNA gaps, a major determinant of PARPi sensitivity in BRCA2-deficient cells. Taken together, these findings suggest that elevated STN1 levels can partially compensate for BRCA2 loss by stabilizing stalled replication forks and limiting ssDNA gap accumulation. Our study uncovers a STN1-dependent pathway of replication stress tolerance that promotes PARPi resistance independently of homologous recombination restoration, highlighting STN1 as a potential biomarker and mechanistic contributor to therapeutic resistance in BRCA2-mutated cancers. - Source: PubMed
Publication date: 2026/05/19
Laghari Zubair AhmedLi NaWang Qi-EnChai Weihang - - Source: PubMed
- The widespread application of PARP inhibitors (PARPis) in epithelial ovarian cancer has led to the emergence of therapy resistance as a critical clinical challenge. To investigate the underlying mechanisms, we perform RNA sequencing of paired patient samples obtained before and after PARPi treatment, revealing a significant upregulation of glycolytic activity following therapy. Olaparib-resistant OVCAR8 and A2780 cells are established by exposure to increasing concentrations of Olaparib, and pharmacological inhibition or knockdown of restores Olaparib sensitivity, with synergistic effects confirmed in patient-derived organoids and xenograft models. Mechanistically, GLUT1 suppression reduces lactate accumulation, subsequently impairing tumor proliferation and DNA repair capacity through downregulation of the DNA repair protein MRE11. These findings establish lactate as a key mediator of PARPi resistance and propose targeting lactate metabolism as a promising combination strategy to improve PARPi efficacy in advanced ovarian cancer. - Source: PubMed
Nie ShuqiPu CongliLiu HongyuPei XuanWang YiLu XiaohangCheng YufanJiang WeiYang Huijuan - Peroxisomal metabolism was long regarded as a housekeeping pathway with minimal involvement in cancer. Nonetheless, accumulating data demonstrate that peroxisomal lipid oxidation critically modulates genome stability and antitumor immunity. The acyl-CoA oxidase (ACOX) family-including ACOX1, ACOX2 and ACOX3-catalyzes the initial oxidative step of peroxisomal fatty acid β-oxidation, and governs lipid metabolism, redox homeostasis, as well as acyl-CoA-related post-translational modifications such as lysine crotonylation. Notably, ACOX2 has gained growing attention for its connections with DNA damage sensing, cGAS-STING activation and anticancer immunity. Dysregulated ACOX2 expression correlates with tumor progression, therapeutic response and clinical prognosis across various cancers, though direct functional evidence varies by tumor type. Mechanistically, ACOX2-related lipid metabolism maintains intracellular redox balance and stress adaptation, with its pathway-specific signaling still poorly defined. In clear cell renal cell carcinoma, ACOX2 binds MRE11 to destabilize the MRN complex, inducing cytosolic DNA buildup and cGAS-STING-mediated type I interferon signaling, while its universal role in other malignancies awaits validation. ACOX2 acts in a context-dependent fashion: it exerts tumor-suppressive effects in liver, prostate and lung cancers, yet facilitates metabolic adaptation and chemoresistance under therapeutic stress. This review summarizes ACOX2 as a key integrator of metabolism, immunity and genome integrity, and highlights its translational potential as a cancer biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/05/23
Zheng MeiguiZhao BaihuiChen XiuyingZhao Ying