CHK2 pThr383 antibody Ab
- Known as:
- CHK2 pThr383 (anti-) Antibody
- Catalog number:
- 1488053
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CHK2 pThr383 antibody
Related genes to: CHK2 pThr383 antibody Ab
- Gene:
- CHEK2 NIH gene
- Name:
- checkpoint kinase 2
- Previous symbol:
- RAD53
- Synonyms:
- CDS1, CHK2, HuCds1, PP1425, bA444G7
- Chromosome:
- 22q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-19
- Date modifiied:
- 2019-04-23
Related products to: CHK2 pThr383 antibody Ab
Related articles to: CHK2 pThr383 antibody Ab
- PARP inhibitors have transformed the way we treat ovarian cancer patients which are homologous recombinant deficient. However, real-world data on response rates is contrasting. We studied the impact of BRCA pathogenic variants (PV) type on progression-free survival (PFS) and overall survival (OS) in high-grade serous ovarian cancer patients treated with PARPi maintenance therapy. - Source: PubMed
Publication date: 2026/07/03
Zeng XingLevin GabrielShabazian LawrieRibeiro ReitanWeber EvanMandilaras VictoriaFoulkes WilliamGilbert Lucy - Performing germline genetic testing of family members following the identification of an individual with a pathogenic variant in a cancer predisposition gene, a process known as cascade testing, is a critical step in maximizing the preventive benefit of genetic testing for hereditary cancer. - Source: PubMed
Publication date: 2026/06/01
Namey EliaHorton CarolynDudley BethCarraway CassidyKomala TimothyMilliard CarrieNamey TaraKarloski EveBrand Randall - Endometrial cancer (EC) is a heterogeneous gynecological malignancy characterized by diverse genetic and epigenetic alterations. This study investigated genetic mutations associated with EC among Kurdish women using next-generation sequencing (NGS). Seventy histopathologically confirmed EC cases were included, and peripheral blood DNA samples were analyzed. Whole-exome sequencing was performed on nine carefully selected cases based on specific clinical and pathological criteria, including early age of onset and/or family history suggestive of hereditary cancer predisposition, following enzymatic fragmentation, adapter ligation, PCR amplification, and targeted capture using biotinylated probes. The analysis identified five potentially significant variants in five genes: CHEK2, MUTYH, PLA2G2A, POLE, and USF3. The detected alterations included a heterozygous deletion in CHEK2 (p. Tyr113del), a homozygous SNP in MUTYH (p. Arg217His), heterozygous SNPs in PLA2G2A (p. Arg77Gly) and POLE (p. Ser2237Arg), and a heterozygous deletion in USF3 (p. Val576del). These findings highlight important molecular features of EC in Kurdish patients and may support future development of targeted therapeutic strategies. Further validation with larger cohorts is recommended. - Source: PubMed
Publication date: 2026/06/25
Hussain Salar SaadiAmin Zahra Abdulqader - Singapore grouper iridovirus (SGIV) is a highly pathogenic virus that causes substantial economic losses in marine grouper aquaculture, and effective antiviral agents are currently lacking. In this study, the anti-SGIV activity of epigallocatechin gallate (EGCG), a natural compound from green tea, was evaluated and its underlying mechanisms were investigated. Cytotoxicity assays showed that EGCG at concentrations up to 12.5 μg/mL was safe for grouper spleen (GS) cells. EGCG treatment reduced viral MCP and VP19 mRNA expression in a dose-dependent manner, indicating its anti-SGIV activity. Mechanistic studies revealed that EGCG directly impaired SGIV particle infectivity and interfered with viral adsorption, entry, and intracellular replication. Network pharmacology analysis identified overlapping genes between EGCG targets and SGIV-induced differentially expressed genes, with enrichment pathways related to cell cycle regulation, particularly the G2/M checkpoint. Further studies showed that SGIV infection upregulated the G2/M checkpoint regulators WEE1 and CHEK2, and EGCG treatment reversed these dysregulations, suggesting that EGCG alleviates SGIV-induced G2/M arrest. In vivo, EGCG treatment significantly reduced viral load in infected groupers and improved survival rate. Collectively, these findings demonstrate that EGCG exerts potent anti-SGIV activity both in vitro and in vivo by directly targeting multiple steps of the viral life cycle and modulating host cell cycle G2/M checkpoint pathways, highlighting its potential as a natural therapeutic agent against SGIV infection. - Source: PubMed
Publication date: 2026/06/26
Zhao TianhongXie JinkunLi Chen-AoLiu MingzhuYu QingHuang LinGao YanxiaZhao MingmingLi JiaxiCai JiaChen HuapuLing FeiQin XiangmouLi Pengfei - Anaplastic thyroid carcinoma (ATC) is an aggressive malignancy with limited treatment options and a poor prognosis. Although vemurafenib targets the BRAFV600E mutation, its therapeutic efficacy in ATC is limited due to poor solubility and insufficient intracellular retention. In this study, vemurafenib was encapsulated in biocompatible polymeric nanocapsules (VEM-PNCs) to enable sustained intracellular delivery and evaluate its time-dependent anticancer effects. We tested the physical and chemical properties of these nanocapsules and examined their biological effects in human ATC 8305C cells. We measured cell death using MTT assays and assessed programmed cell death (apoptosis) by flow cytometry with Annexin V and Propidium Iodide, Hoechst staining, and microscopic examination. We also measured gene expression changes related to apoptosis and DNA damage using RT-qPCR. The VEM-PNCs produced a delayed onset but prolonged cytotoxic activity compared with free vemurafenib, consistent with controlled intracellular drug release rather than enhanced immediate cytotoxic potency. Empty nanocapsules showed minimal cytotoxicity. Following longer incubation periods, VEM-PNC-treated cells exhibited a higher proportion of apoptotic cells than cells treated with free vemurafenib, suggesting prolonged intracellular drug exposure. These effects were associated with up-regulation of ATM, CHEK2, and TP53, and down-regulation of MDM2 and MDM4, indicating activation of DNA damage response (DDR) and p53-associated signaling pathways. Increased expression of Caspase-3, -8, -9 and BAD suggested that both extrinsic and intrinsic apoptotic pathways were activated. Microscopic examination confirmed apoptotic features, including condensed nuclei and membrane blebbing, in cells treated with VEM-PNCs. These findings suggest that delivering vemurafenib in polymeric nanocapsules produces delayed but sustained cytotoxic and apoptotic effects in ATC cells in vitro, warranting further investigation of this nanocarrier approach for thyroid cancer treatment. Altogether, the biological results reported in this study are derived from in vitro experiments and require further validation in in vivo models. - Source: PubMed
Publication date: 2026/06/25
Heidari TaherehMotalleb GholamrezaRahdar Abbas