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
- Synthetic lethality has reshaped oncology, particularly in tumours with defects in DNA damage response (DDR) pathways, yet therapeutic strategies centred on canonical DDR targets, including poly(ADP-ribose) polymerase (PARP), ataxia telangiectasia and Rad3-related protein (ATR), checkpoint kinase 1 (CHK1) and Wee1 G2 checkpoint kinase (WEE1), remain constrained by resistance, toxicity and biological heterogeneity of DDR alterations. Emerging evidence indicates that DDR deficiency extends beyond impaired DNA repair to generate interconnected stress phenotypes involving replication fork instability, chromosomal instability, transcriptional and cell-cycle dysregulation, oxidative/proteotoxic stress and metabolic imbalance. These states may increase tumour-cell reliance on kinases that are not canonical DNA repair enzymes or proximal DDR sensors, here referred to as non-canonical DDR-associated kinases. In this review, we examine the mechanistic rationale and translational potential of targeting kinases that regulate mitosis, transcriptional adaptation, checkpoint signalling, stress responses and metabolic homeostasis in DDR-defective tumours. We distinguish kinase dependencies supported by direct DDR-context-specific vulnerability or PARP inhibitor sensitisation from those whose relevance remains primarily mechanistic or hypothesis-generating and propose a shift from genotype-based patient selection toward functional stress phenotyping that integrates DNA repair capacity with replication stress, chromosomal instability, transcriptional conflict and the metabolic state. Finally, we evaluate pharmacological strategies, including rational combinations, allosteric modulation, polypharmacology and targeted protein degradation, and highlight the need for biomarker-guided clinical translation. - Source: PubMed
Publication date: 2026/09/17
Masi MircoVarignani GiuliaCavalli AndreaGirotto Stefania - High-grade serous carcinoma (HGSC) of tubo-ovarian origin is an aggressive malignancy in need of new treatment options. At the molecular level, HGSC is characterized by genomic instability, including nearly universal mutations, copy number alterations, and chromothripsis, which elevate replication stress. These fundamental alterations result in tumor cell dependence on the G2/M checkpoint for survival, thus revealing this checkpoint as a potential therapeutic target. In this review, we discuss the normal cell cycle progression and checkpoints as well as the regulation of DNA replication, and we consider how replication stress in HGSC leads to a dependence on the G2/M checkpoint. We then present information on the current state of targeted therapy development for HGSC including clinical trials and the role of biomarkers in optimal patient selection. Thus, targeting the G2/M checkpoint is driven by sound molecular rationale and may yield clinical benefit in patients with HGSC, but will likely require careful patient selection and consideration of treatment toxicities. - Source: PubMed
Publication date: 2026/09/17
Tian ZhiyuMcLean Karen - : Osteoarthritis (OA) is a whole-joint disease, and cellular senescence is one of several processes associated with cartilage degeneration. This study aimed to identify senescence-associated differentially expressed genes in established OA and to examine checkpoint-related candidates without assuming a causal checkpoint-imbalance mechanism. : Five Gene Expression Omnibus (GEO) datasets spanning articular-cartilage tissue and primary cartilage-derived chondrocytes (GSE57218, GSE117999, GSE114007, GSE246425, and GSE169077) were integrated as a training cohort; the meniscus dataset GSE98918 was reserved as an independent cross-tissue validation cohort. OA-associated differentially expressed genes (DEGs) were intersected with CELLAGE genes. Enrichment, protein-protein interaction, transcription-factor, competing endogenous RNA, drug-enrichment, and molecular-docking analyses were performed. CDK6 and WEE1 expression was evaluated in IL-1β-treated human C28/I2 chondrocytes by RT-qPCR and representative Western blotting. : Forty-one senescence-associated DEGs were identified, and seven network-central genes (CDKN1A, CDK6, WEE1, NFKB2, ID1, RBL2, and IGFBP7) were prioritized. CDKN1A, CDK6, and WEE1 were reduced in OA-associated meniscal samples in GSE98918; within-dataset ROC analyses yielded AUCs of 0.931, 0.882, and 0.792, respectively. In IL-1β-treated C28/I2 cells, WEE1 mRNA decreased whereas CDK6 mRNA increased; representative immunoblots showed concordant qualitative trends. Berberine- and folic acid-related docking findings were computational only. : Checkpoint-related gene expression is associated with senescence-linked transcriptomic changes in established OA. The discordant CDK6 results between clinical tissue datasets and an acute inflammatory cell model do not establish stage-dependent regulation. The present data also do not demonstrate p53-mediated CDKN1A activation, checkpoint failure, cell-cycle arrest, or cellular senescence; these hypotheses require dedicated functional experiments. - Source: PubMed
Publication date: 2026/08/26
Liao Chang-ShengJu Yu-CanWang Min-XiaoLong ChengLan Feng-Jun - Bifunctional genomic loci can produce both coding and noncoding outputs, yet the proteins encoded by many such loci remain unexplored. Here, we identify MSEP, a previously uncharacterized ∼54-kDa protein translated from an open reading frame embedded within the antisense RNA locus ARHGEF17-AS1. MSEP localizes to the mitotic spindle and spindle poles, and disruption of its start codon increases spindle abnormalities. MSEP interacts with the spindle-assembly factor TPX2, and its depletion is accompanied by reduced TPX2 abundance. MSEP undergoes cell-cycle-dependent phosphorylation that is regulated by Aurora A and WEE1. Depletion of MSEP is also associated with diminished Aurora A abundance at spindle poles. Genetic uncoupling of MSEP translation from ARHGEF17-AS1 RNA expression supports largely distinct protein- and RNA-mediated pathways that converge on spindle-pole integrity. Together, these results support a bifunctional-locus model in which ARHGEF17-AS1 RNA and its encoded protein, MSEP, contribute to mitotic spindle integrity through distinct, parallel pathways. - Source: PubMed
Publication date: 2026/09/24
Mahale SagarChikne VaibhavAdithya NitinMohamed Mohamed ShamsudiinSetia MeenakshiSjövall DanielPrajapati BharatHallqvist AndreasKanduri MeenaKanduri Chandrasekhar - Growing evidence indicates that dysregulation of circadian clock genes and cell cycle regulators plays a role in the pathogenesis of malignancies. BMAL1, a core circadian clock gene, and WEE1, a key regulator of the G2/M cell cycle checkpoint, are involved in controlling cell proliferation and maintaining genomic stability. The present study aimed to evaluate the expression pattern of these two genes in children with acute myeloid leukemia. - Source: PubMed
Publication date: 2026/09/25
Oraei Sajjadi KimiaAyatollahi HosseinSheikhi MaryamAhmadi Mohammad Hossein