CHEK1 Antibody - middle region (ARP30333_T100)
- Known as:
- CHEK1 Antibody - middle region (ARP30333_T100)
- Catalog number:
- arp30333_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CHEK1 Antibody - middle region (ARP30333_T100)
Related genes to: CHEK1 Antibody - middle region (ARP30333_T100)
- Gene:
- CHEK1 NIH gene
- Name:
- checkpoint kinase 1
- Previous symbol:
- -
- Synonyms:
- CHK1
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-21
- Date modifiied:
- 2011-11-11
Related products to: CHEK1 Antibody - middle region (ARP30333_T100)
Related articles to: CHEK1 Antibody - middle region (ARP30333_T100)
- Checkpoint kinase 1 (CHK1), a key regulator of cell cycle checkpoints, plays a central role in the DNA damage response network, serving as a critical mediator that links DNA damage detection to DNA repair mechanisms. In recent years, several other cellular functions of CHK1 have gradually been discovered. As well as monitoring genomic integrity, CHK1 coordinates the timing of DNA replication with the availability of metabolic resources. This prevents unscheduled DNA synthesis from exceeding the cell's metabolic capacity and causing DNA damage. CHK1 activity also contributes to tumour immune surveillance and the modulation of immune cell infiltration and immune escape mechanisms within the tumour microenvironment. Furthermore, CHK1 is involved in the regulation of differentiation and epigenetics. This perspective on CHK1 provides a strategy foundation for next-generation combinatorial therapies. Indeed, the data presented herein underscores the potential of novel therapeutic strategies that target diverse aspects of tumour biology in a simultaneous manner. Despite the current lack of clinically approved CHK1 inhibitors, the pleiotropic roles of this kinase make it an attractive and promising target for new cancer therapies. The present review aims to analyze the structural and functional aspects of CHK1, with a particular focus on its "non-canonical" functions. - Source: PubMed
Publication date: 2026/05/21
Franza MariaMelfi AuroraAcconcia FilippoMasi Alessandra di - Breast cancer burden is increasing day by day. The identification of novel genetic markers based on polymorphism and expression analysis is necessary to reduce the suffering of patients. - Source: PubMed
Publication date: 2026/05/29
Mehmood AzharMahjabeen IshratNisar AsifUmar MuhammadKayani Mahmood Akhtar - Esophageal squamous cell carcinoma (ESCC) is aggressive with poor prognosis, frequently driven by chemotherapy resistance. Kinesin family member 18B (KIF18B) is implicated in tumor progression, but its role in ESCC chemoresistance remains unclear. To investigate KIF18B's clinical relevance and mechanistic contribution to oxaliplatin resistance in ESCC, KIF18B expression was analyzed in TCGA data, ESCC cell lines/tissues (qPCR, Western blot, IHC), and correlated with survival (Kaplan-Meier). Results showed that, KIF18B was significantly elevated in ESCC and correlated with shorter overall/progression-free survival. Knockdown reversed oxaliplatin resistance, reducing IC50 from 8.5 µM to 3 µM, restoring apoptosis, and inducing G2/M arrest. Silencing suppressed the ATR/CHK1 pathway (reduced p-ATR, p-CHK1, WEE1, CDC25A) and increased γH2AX foci. Co-IP confirmed KIF18B-ATR interaction, suggesting stabilization of DNA damage signaling. In vivo, KIF18B knockdown synergized with oxaliplatin, achieving > 80% tumor suppression and reduced Ki-67/p-ATR/p-CHK1 levels. In conclusion, KIF18B is a prognostic biomarker and therapeutic target in ESCC. Its inhibition overcomes oxaliplatin resistance by disrupting KIF18B-ATR interaction and ATR/CHK1-mediated DNA repair. Combining KIF18B targeting with chemotherapy or ATR inhibitors represents a promising strategy for refractory ESCC. - Source: PubMed
Publication date: 2026/05/27
Liu WeiWang QianruTan XiaoCao ChunyuTian Bole - Tyrosine kinase inhibitors represent the most effective and long-lasting treatment currently available for aggressive thyroid cancers, but in some patients the response is poor or absent. Recently, we demonstrated that the response to Lenvatinib is associated with alterations in gene or protein. Aiming to find a novel therapeutic strategy for aggressive thyroid cancers, we investigated the DNA damage response pathway, where p53 plays a crucial role, and tested its inhibition through synthetic lethality or stress sensitization strategies. - Source: PubMed
Publication date: 2026/05/08
Manzo AlessandroGrassi Elisa StellariaBorghi Maria OriettaColombo CarlaPersani LucaCirello Valentina - Hepatocellular carcinoma (HCC) metastasis often threatens patient survival. However, there is still a lack of effective treatments to tackle this problem. Ruanjianhugan tablets (hepatoprotective and fibrolytic tablets), a traditional Chinese herbal compound, have demonstrated potential in repressing the progression of HCC. However, the exact active ingredients and mechanisms behind its effects are not yet fully understood. In this study, we leveraged network-pharmacology tools to screen the key bioactive constituent-calycosin (Cal)-from this compound formula and predicted it as the target for the downstream gene checkpoint kinase 1 (CHEK1) in HCC cells. Subsequent cellular thermal shift assay (CETSA) verified that Cal bound CHEK1. , CCK-8, colony-formation, Transwell and Western-blot assays showed that Cal markedly suppressed HCC-cell proliferation, colony formation, migration, invasion and epithelial-to-mesenchymal transition. In xenograft nude-mouse and tail-vein lung metastasis models, exogenous Cal bound CHEK1 and thereby inhibited HCC metastasis and tumor growth. Collectively, these results not only establish Cal as the core pharmacodynamic component of Ruanjianhugan tablets but also unveil a novel Cal-CHEK1 axis underlying anti-HCC metastasis. - Source: PubMed
Publication date: 2026/05/21
Wan PeiqiLiu ZhihongLi KaiWen ZhangNing QiuyueXiao Fang