WEE1
- Known as:
- WEE1
- Catalog number:
- 000227A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- WEE1
Related genes to: WEE1
- 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
Anti-Mouse WEE1 (KIBB3098), Rabbit PolyclonalAnti-Mouse WEE1 (KIBB3098), Rabbit Polyclonalanti-Wee1anti-Wee1anti-Wee1anti-Wee1anti-Wee1 (5B6)anti-Wee1 (5B6)anti-Wee1 type: Primary antibodies host: Mouseanti-Wee1 type: Primary antibodies host: RabbitBovine Wee1-like protein kinase 2(WEE2) ELISA kitCanine Wee1-like protein kinase 2(WEE2) ELISA kitCanine Wee1-like protein kinase 2(WEE2) ELISA kitCanis familiaris,Canis lupus familiaris,Dog,WEE1B,Wee1B kinase,Wee1-like protein kinase 1B,Wee1-like protein kinase 2,WEE2Chicken WEE1 homolog 2 (S. pombe) (WEE2) ELISA kit, Species Chicken, Sample Type serum, plasma Related articles to: WEE1
- Transarterial chemoembolization (TACE) is the standard treatment for patients with intermediate-stage hepatocellular carcinoma (HCC), yet nearly half of treated patients fail to achieve durable benefit, and reliable biomarkers enabling early therapeutic stratification are still lacking. Treatment response is typically assessed by imaging one month after TACE and at three-month intervals, potentially delaying timely access to alternative therapies in non-responding patients. Circulating microRNAs (miRNAs) represent promising biomarkers due to their stability in body fluids and ease of detection. Here, we evaluated circulating miR-22 as an early predictor of TACE non-responder status and as a mechanistically relevant therapeutic target. Circulating miR-22 levels were measured by microarray and quantitative RT-PCR in three independent cohorts of early-to-intermediate-stage HCC patients undergoing TACE. Circulating miR-22 increased significantly in non-responders as early as 48 h after treatment, and fold changes consistently predicted treatment failure across two independent validation cohorts. Mechanistically, we identified the G2/M checkpoint kinase WEE1 as a direct functional target of miR-22. Modulation of the miR-22/WEE1 axis affected cell-cycle progression, proliferation, apoptosis, and DNA damage response in HCC cell lines and xenograft models. Under hypoxia-mimicking conditions combined with doxorubicin exposure, pharmacological inhibition of WEE1 induced mitotic catastrophe in highly proliferative miR-22-silenced cells. Collectively, these findings identify early post-TACE elevation of circulating miR-22 as a biomarker of non-response and highlight the miR-22/WEE1 axis as a potential target for precision treatment strategies in HCC. - Source: PubMed
Publication date: 2026/04/19
Gramantieri LauraVianello ClaraLeoni IlariaGalvani GiuseppeMonti ElisaBella MarcoMarisi GiorgiaSalamon IreneFerracin ManuelaRavegnini GloriaGiovannini CatiaStefanelli ClaudioLazzari Maria LauraPiscaglia FabioCoada Camelia ABassi CristianNegrini MassimoCasadei-Gardini AndreaFoschi Giuseppe FrancescoTrerè DavideFornari Francesca - Homologous recombination (HR) deficiency (HRD) and replication stress (RS) are increasingly recognized as interconnected hallmarks of genomic instability in cancer, offering promising avenues for therapeutic targeting. As novel combination therapies targeting these hallmarks continue to emerge, understanding how these processes interact in therapeutic contexts and comparing the relative efficacy and toxicity of combination therapy is critical in advancing precision oncology. - Source: PubMed
Publication date: 2026/04/26
Ozmen Tugba YFrankston Connor MRames Matthew JOzmen FurkanYardimci Galip GMills Gordon B - Herein, we report the discovery of APO-50815 (14), a potent and selective thietane-3-ol WEE1 inhibitor. When tested against TP53-mutated colorectal cancer (CRC) patient-derived organoids (PDOs) grown from peritoneal and liver metastases, 14 exhibited outstanding anticancer efficacy, surpassing previously reported branched alkane counterpart 3, as well as clinical candidates AZD1775 (1) and ZN-c3 (2). Against primary CRC organoids with diverse TP53, BRAF and KRAS mutation profiles compared with patient-matched normal colon organoids, 14 exhibited selectively potent activity, yielding exceptionally high TI values (129-238) that highlight a substantial therapeutic window for potential cancer treatment. Against primary CRC PDOs (TP53-WT, BRAF-V600E, KRAS-WT), 14 profoundly elevated DNA damage and replication stress compared to 1, while amplifying cellular apoptosis, confirming a broadly similar but superior mode of action. Owing to its highly selective and exemplary anticancer efficacy, 14 represents a valuable tool compound for drug testing investigations against primary and metastatic CRCs, especially in the context of PDOs. - Source: PubMed
Publication date: 2026/04/05
Syphers Joel LWright Josephine Ade Nys RebekahSilva Tharindie NVrbanac LauraBarratt Kate RLeeflang JuliaHasan Sadia TThomson Sophie FKumar AdarshKrämer AndreasLenz ChristopherGee Yi SingChang AesonYoung SavannahSloan Erica KKnapp StefanWorthley Daniel LMukherjee SiddharthaStockton KieranPriebbenow Daniel LWoods Susan LBaell Jonathan B - Li-Fraumeni syndrome (LFS), driven by germline TP53 mutations, confers a markedly elevated risk of osteosarcoma (OS), yet the mechanisms beyond TP53 remain insufficiently defined. By integrating multi-omics analyses and in vitro validation, we identify SCL-interrupting locus (STIL) as a pivotal hub linking LFS to OS progression. We reveal that STIL negatively regulates p53 protein stability in a manner independent of TP53 mutation status, indicating that STIL can promote tumorigenesis by dampening p53 pathway activity and stability. Importantly, STIL displays genetic-context-dependent oncogenicity: it supports stemness across OS models, but more strongly drives invasion and metastatic potential in TP53-mutant backgrounds. Specifically, STIL is highly expressed in a population of high-stemness malignant cells (Pro-OSCs), where it maintains stemness and promotes bone destruction by activating PTN-NCL and FN1-CD44 pathways, while simultaneously remodeling the immune microenvironment via MIF and APP signaling to evade immune surveillance. Additionally, WEE1 inhibitors may represent a targeted vulnerability in STIL-high OS. In summary, the relationship between TP53 and STIL is not a simple linear upstream-downstream cascade, but reflects a highly context-dependent regulatory dynamic. STIL exerts oncogenic effects by regulating p53 stability and driving a "stemness-invasive" phenotype in the context of TP53 mutations. This also provides novel biomarkers and intervention targets for precision therapy. - Source: PubMed
Publication date: 2026/04/20
Qiao YuHao JincenYuan FahuCurto-Vilalta AnnaTang Longvon Eisenhart-Rothe RüdigerHinterwimmer Florian - Dual inhibition of PKMYT1 and WEE1, key G2/M checkpoint kinases that phosphorylate CDK1 at T14 and Y15, offers a strategy for tumors with abrogated G1/S checkpoint and high replication stress. Building on our prior PKMYT1 chemotype, we designed 1,7-naphthyridinone derivatives by displacing crystallographic water (core 5'-N-Asp251) and adding a 7'-ring nitrogen to retain physicochemical properties. 5'-Site structure fine-tuning enhanced WEE1 engagement while preserving the PKMYT1-preferred hinge flip and superior kinome selectivity. Optimization identified compound with single-digit nM PKMYT1 NanoBRET and sub-μM WEE1 NanoBRET potency, translating to pCDK1 T14 IC50 4.9 nM and pCDK1 Y15 0.186 μM in HCC1569 cells. Kinome profiling confirmed favorable selectivity. In colorectal cancer organoids, outperformed our prior PKMYT1 inhibitor (), RP-6306, and WEE1 inhibitor AZD1775, with efficacy correlating to improved WEE1 activity. Compound also showed favorable ADME and early safety profiles, supporting dual checkpoint targeting in checkpoint-deficient cancers. - Source: PubMed
Publication date: 2026/04/20
Chen BoLiu XiaofengXu JiasuZhao DanTang YangXu ZhihengYang JuneLi ChihoChen ShuaiZhu SiningWang SummerYao XiangyuYan ZhipengWeng MinruiWang PanMa YannaWang XujunChen Wenli KellyTu YifanQiu HongxiaYang JuhaoJiang TianyiJi YingShen Hong CZhu WeiTan XuefeiWu Jun