CHK1
- Known as:
- CHK1
- Catalog number:
- 000210A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CHK1
Related genes to: CHK1
- 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: CHK1
Related articles to: CHK1
- Endocrine resistance remains a major challenge in hormone receptor-positive (HR+) breast cancer (BC), where up to 70% of tumours overexpress HER3, a receptor associated with poor prognosis and therapeutic resistance. HER3-DXd (patritumab deruxtecan) is currently under clinical investigation for HER3-expressing metastatic BC. However, strategies to further enhance its efficacy, particularly in endocrine therapy-resistant settings, are urgently needed. We hypothesised that targeting ATR, a key regulator of DNA damage repair (DDR), potentiates HER3-DXd in HER3+/HR+ BC, including tamoxifen-resistant (TMR) disease. - Source: PubMed
Publication date: 2026/04/15
Xie XuemeiLee JangsoonGi Young JinPoullikkas ThanasisFuson Jon AFan Pang-DianFukui Jami ATripathy DebuUeno Naoto T - Unclassified round cell sarcomas (URCS) are a rare sarcoma subtype. Systemic treatment options for advanced URCS are limited, primarily consisting of radiotherapy and chemotherapy, while the efficacy and prerequisites for immunotherapy in URCS remain unclear. A better understanding of factors influencing the response to immunotherapy in URCS may facilitate the development of combination treatment strategies to prolong patient survival. This study reports a 60-year-old male patient with gallbladder URCS who was administered a combination of chemotherapy, bevacizumab, and pembrolizumab, followed by radiotherapy, achieving a progression-free survival of 11 months. This result supports the potential application of immunotherapy in advanced URCS. The patient exhibited vascular endothelial growth factor receptor amplification, mutations in CHEK1, ERCC3, and TP53, deletion of CD274 (gene of PD-L1), and microsatellite stability. These findings suggest that immunotherapy may be beneficial to URCS patients with low PD-L1 expression and microsatellite stability, when accompanied by immunotherapy-associated genetic alterations. - Source: PubMed
Publication date: 2026/04/08
Wang DandanLi TingWang XuanyiWang YingXu GuixuanXiao XueHu LanlinXu Chuan - Glioblastoma is a highly invasive primary brain tumor with a poor prognosis, highlighting the need for new therapeutic strategies. Toxins derived from have attracted attention for their potential anticancer activity. This study evaluated the anticancer and cytotoxic effects of crude venom on two commonly used glioblastoma cell lines (U251 and LN229), which mirror the phenotype of primary tumors. Cell viability and proliferation were assessed using the CCK-8 assay and colony formation assay, while cell migration and invasion capabilities were detected via wound healing assay and Transwell assay. Annexin V/PI staining and PI-based cell cycle analysis indicated that the crude venom significantly induced cell apoptosis and caused S-phase arrest. Proteomic analysis combined with GO and KEGG enrichment analyses as well as bioinformatics approaches showed that crude venom inhibits glioblastoma cell proliferation by downregulating the expression of CDK2, RRM2, and CHEK1, thereby hindering cell cycle progression and regulating the p53 signaling pathway. Notably, the downregulation of these key glioblastoma-related target genes was validated by qPCR. In addition, network pharmacology analysis indicated that several peptide families present in the sea anemone crude venom, including ShK peptides, inhibitor cystine knot (ICK) peptides, and EGF-like peptides, exhibit notable antitumor potential. Combined with AlphaFold2-based structural modeling and molecular docking, these analyses further elucidated the potential molecular mechanisms underlying their interactions with key targets, such as MD-381 with RRM2, MD-322 with CDK2, and MD-429 with CHEK1. Collectively, these findings highlight the therapeutic potential of crude venom and lay a foundation for the subsequent isolation of novel peptides and their further development in glioblastoma treatment. - Source: PubMed
Publication date: 2026/02/26
Lin LiminHuang MeilingYang WantingHua ZiqiangChen ZhenHe PanminMao KailinCheng ShuanghuaiMa LinlinCui ShuaiyingYi BoGao Bingmiao - CHK1, a key serine/threonine kinase, is essential for cell cycle progression and genome maintenance in response to DNA damage and/or replication stress. However, its functions during normal DNA replication remain to be defined. Here, we employed the dTAG system to achieve rapid and selective CHK1 depletion in cells and examined the consequences of its acute loss. CHK1 degradation led to rapid cell death, with significant loss of viability within 16 h and complete lethality by 48 h, indicating critical roles of CHK1 during normal DNA replication. Rescue experiments demonstrated that only full-length, catalytically active CHK1 could restore cell survival, emphasizing the essential role of its kinase function and ATR-dependent phosphorylation. CHK1 depletion triggered extensive DNA damage, as evidenced by increased γH2AX and RPA2 phosphorylation, and caused S-phase arrest, replication fork collapse, and failure to enter mitosis. Interestingly, cells arrested at the G1/S boundary, which do not undergo DNA replication, were still sensitive to CHK1 depletion. These data reveal a critical role of CHK1 in suppressing replication fork progression even in the absence of DNA replication. Thus, our results highlight CHK1's indispensable role in the management of replication fork stability and cell cycle progression, providing a refined mechanistic understanding of its function during normal cell proliferation. - Source: PubMed
Publication date: 2026/03/26
Li SitingZhu DandanTang MengfanHuang MinFeng XuNie LitongZhang HuiminYin LingKeast SarahYang ChangMa TiantianChen Junjie - This study aims to systematically investigate the molecular mechanisms through which parabens may contribute to head and neck squamous cell carcinoma (HNSCC) carcinogenesis using integrated network toxicology and molecular docking. - Source: PubMed
Publication date: 2026/03/23
Zhao LeiYang JianwangLiu TaoCao HuanYu MiaomiaoWang Baoshan