WEE1 (Phospho-Ser642) Antibody
- Known as:
- WEE1 (Phospho-Ser642) Antibody
- Catalog number:
- 11706
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- WEE1 (Phospho-Ser642) Antibody
Related genes to: WEE1 (Phospho-Ser642) Antibody
- Gene:
- WEE1 NIH gene
- Name:
- WEE1 G2 checkpoint kinase
- Previous symbol:
- -
- Synonyms:
- WEE1A
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-06
- Date modifiied:
- 2016-07-28
Related products to: WEE1 (Phospho-Ser642) Antibody
Related articles to: WEE1 (Phospho-Ser642) Antibody
- In our view, molecular classification should guide, but not independently determine, treatment for endometrial cancer. The four major molecular subtypes-POLE-mutated (POLEmut), mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H), p53-abnormal/copy-number-high (p53abn/CNH), and no specific molecular profile/copy-number-low (NSMP/CNL)-should be interpreted together with histological type, tumor grade, stage, myometrial invasion, lymphovascular space invasion, comorbidities, fertility goals, treatment accessibility, and patient preferences. For advanced or recurrent dMMR/MSI-H disease, we favor immune checkpoint inhibition because this subtype has the clearest predictive evidence, with immunotherapy increasingly incorporated into first-line treatment. For tumors harboring a confirmed pathogenic POLE exonuclease-domain mutation, we support careful consideration of adjuvant treatment de-escalation, while avoiding de-escalation based on non-pathogenic variants, variants of uncertain significance, or molecular classification alone in advanced-stage disease. We regard p53abn/CNH tumors as a high-risk phenotype requiring appropriately intensive multimodality treatment; human epidermal growth factor receptor 2-targeted therapy, DNA damage response-directed strategies, WEE1 G2 checkpoint kinase inhibition, and antibody-drug conjugates should be considered according to tumor biomarkers, treatment setting, and evidence strength. NSMP/CNL should not be managed as a uniform residual category. Secondary stratification using estrogen receptor/progesterone receptor status, L1 cell adhesion molecule expression, catenin beta 1 alterations, and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway alterations may identify hormone-sensitive, high-risk, and potentially targetable subgroups. In fertility-sparing management, molecular findings may refine counseling and surveillance but should not replace established eligibility criteria. At recurrence or progression, repeat biopsy and biomarker reassessment should be considered when clinically feasible and likely to alter treatment. - Source: PubMed
Publication date: 2026/08/27
Zhou QingyuFu WenxiuZhang QianshuoTian XiaoluZhang Zhengmao - PKMYT1 is a WEE-family G2/M cell cycle checkpoint kinase commonly overexpressed in a broad spectrum of human malignancies. WEE1 exclusively phosphorylates CDK1 at Tyr15, whereas PKMYT1 targets both Thr14 and Tyr15. Unlike WEE1 inhibition, PKMYT1 suppression triggers synthetic lethality with . Nearly all disclosed PKMYT1 inhibitors so far fall into structural analogs originating from , making the discovery of PKMYT1 inhibitors with chemotypes distinct from crucial. The compounds were structurally optimized using CADD, synthesized, and characterized by H NMR, C NMR, HRMS, and HPLC. They were then assessed for kinase binding affinity via the LanthaScreen Eu kinase binding assay, for cellular activity using the CCK-8 assay, and for cell-cycle distribution by flow cytometry, along with investigations into related mechanisms. This study yielded 24 compounds of 2-aminopyrimidine through substituent derivatization of the pyrimidine scaffold. Among these derivatives, exhibited potent kinase binding affinity against PKMYT1 (IC = 0.86 nM) and demonstrated strong anti-proliferative activity against high-amplification OVCAR3 cells and HCC1569 cells (IC = 1.52 μM, IC = 0.66 μM). Additionally, it showed some selectivity towards A549 and HEK293T cells, with SI values of 4.31 (A549/OVCAR3), 9.92 (A549/HCC1569), 2.04 (HEK293T/OVCAR3), and 4.70 (HEK293T/HCC1569). Compound dose-dependently suppressed clonogenicity and triggered S-phase cell cycle blockade. Pharmacokinetic studies showed moderate hepatic microsomal stability (t = 32.2 min). Molecular dynamics simulations indicated a favorable binding mode between compound and PKMYT1 (docking score: -9.322 kcal/mol). is a promising highly potent tool compound that provides a clear direction for the future optimization of PKMYT1 inhibitors. - Source: PubMed
Publication date: 2026/08/21
Yuan ShizheSu ChuanxuZhang ChenxiZhang HaoyuYu JinyuLiu NianFan CunzhengGao ZixuanLuo ZiruiSun YinZhao DongmeiCheng Maosheng - Molecular response (MR) based on circulating tumor DNA (ctDNA) is emerging as a promising early biomarker of treatment efficacy in solid tumors; however, its clinical utility in high-grade serous ovarian cancer (HGSOC) remains to be established. This study evaluates the potential predictive value of ctDNA-based MR in with patients HGSOC treated with the WEE1 inhibitor azenosertib. - Source: PubMed
Publication date: 2026/08/26
Jeong JinkilMa JianhuiAbed MonaChung HeekyungKim DorisMolden NandiniRajendran DivyaShim ChanghwanJandial Danielle DSimpkins FionaMeric-Bernstam FundaRandall Leslie MLackner Mark RHarismendy Olivier - DNA replication stress threatens genome stability, but how plants respond to this challenge remains unclear. Here we show that the evolutionarily conserved polymerase-associated factor 1 complex (PAF1C) is required for the replication stress response in Arabidopsis. Plants lacking functional PAF1C are hypersensitive to replication stress-inducing agents. Mechanistically, we reveal a plant-specific pathway in which the stress-activated kinase WEE1 phosphorylates PAF1 to prevent its protein degradation, a regulatory mechanism absent in yeast. By contrast, we uncover a conserved pathway in which the replication factor C (RFC) complex recruits PAF1C to stalled replication forks, where PAF1C in turn recruits the E2 ubiquitin-conjugating enzymes UBC1/2 and the E3 ubiquitin ligases HUB1/2 to promote histone H2B monoubiquitination, thereby stabilizing the forks. Collectively, our findings suggest that PAF1 regulates replication stress responses by integrating a plant-specific protein stability control mechanism (WEE1-PAF1) with a conserved recruitment mechanism (RFC-PAF1-UBC1/2-HUB1/2). This work establishes a new function for PAF1C and expands the mechanistic understanding of WEE1 and the RFC complex in the replication stress response. - Source: PubMed
Publication date: 2026/08/24
Li CunliangGuo YuyuWang ZiyingZheng HaoweiDeng JingYan ShunpingWang Lili - Cervical cancer remains a major threat to women's health worldwide, and reliable serum biomarkers for early detection and therapeutic stratification remain limited. Human wings-apart-like (hWAPL) protein has been implicated in cervical carcinogenesis, but its diagnostic and clinical value has not been fully elucidated. To address this gap, this study integrated public multi-omics datasets, including The Cancer Genome Atlas, GEPIA2, the Human Protein Atlas, and single-cell transcriptomic data, to characterize hWAPL expression, clinicopathological associations, immune infiltration, co-expression networks, post-translational modifications, and drug sensitivity predictions. These findings were evaluated in an independent single-center serum cohort comprising 89 patients with histologically confirmed cervical squamous cell carcinoma and 89 healthy female controls. Serum hWAPL and squamous cell carcinoma antigen (SCC) levels were measured, and diagnostic performance was assessed by receiver operating characteristic curve analysis. In silico, hWAPL was broadly upregulated across multiple malignancies, particularly cervical cancer, enriched in malignant epithelial cells and monocytes/macrophages, and associated with shorter progression-free interval, predicted reduced sensitivity to cisplatin, paclitaxel, and 5-fluorouracil, and predicted sensitivity to MCL-1 and Wee1 inhibitors. In the serum cohort, hWAPL levels were significantly higher in patients than controls and discriminated cervical cancer with an area under the curve of 0.961, exceeding SCC alone. Combining hWAPL with SCC further improved diagnostic performance (area under the curve, 0.974; sensitivity, 93.3%; specificity, 95.5%). These findings suggest that serum hWAPL is a potential novel diagnostic biomarker for cervical squamous cell carcinoma whose performance is enhanced by SCC, whereas the observed associations with chemoresistance and immune microenvironment remodeling are hypothesis-generating and require experimental confirmation. - Source: PubMed
Publication date: 2026/08/21
Gao MinghuaWu LingzhiLiu MengLiu Wenkang