Ask about this productRelated genes to: CHK1 antibody
- 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 antibody
Related articles to: CHK1 antibody
- Breast cancer (BC) is one of the most diagnosed malignancies and a leading cause of cancer-related mortality among women worldwide, thereby posing a substantial threat to women's health worldwide. However, clinically robust diagnostic biomarkers with high sensitivity and specificity, as well as well-validated molecular targets for targeted therapy, remain limited. - Source: PubMed
Publication date: 2026/03/30
Wang ZifuHou JinqiChen YiminLi JundiVengusamy Sivakumar - The use of postmortem (autopsy) material in fundamental and applied biomedical research significantly facilitates the collection of biomaterial for statistically robust sample cohorts. However, natural adaptive processes to developing cellular stress in the early postmortem period, caused by oxygen and nutrient deprivation, trigger the activation of numerous genes promoting cell survival under stress. Many of these activated pathways are also crucial for tumor cell survival in vivo, as evidenced by various transcriptomic studies. This study aimed to investigate the potential influence of postmortem interval (PMI) duration on gene expression in normal and tumor tissues. Using a model of chemically induced hepatocellular carcinoma in mouse liver, we comparatively analyzed the dynamics of transcript levels for several genes (BRCA1, BRCA2, CHEK1, CHEK2, ATM, CDK12) in paired samples of normal and tumor tissue over a 24-h PMI using RT-qPCR. In normal tissue, gene expression increased significantly, while tumor tissue demonstrated relative transcriptional stability, with no substantial changes in the studied transcript levels. A critical finding was the observed convergence of expression profiles: initial differences between the tissues were completely eliminated by 24 h PMI. This pattern developed despite formally adequate RNA quality (RQN) and the absence of clear signs of progressive autolysis in histology, indicating the insufficiency of standard quality criteria for detecting postmortem changes. These findings collectively underscore the critical importance of minimizing and controlling PMI during the biobanking of oncological samples for reliable transcriptomic research. - Source: PubMed
Publication date: 2026/04/16
Buyko Evgeny EPerina Ekaterina ASobakin Danil STsyganov Matvey MVasilchenko Dmitry VVtorushin Sergey VUfandeev Alexander ADiksas Elena BKaidash Olga AHmelevskaya Ekaterina SParochkina Ekaterina VPopov Igor AIvanov Vladimir VPekov Stanislav IUdut Elena V - Identifying cancer driver genes (CDGs) remains a central challenge in cancer genomics, as frequency-based mutation approaches often miss rare but functionally important regulators. We present PICDGI, a computational framework that predicts driver-like regulatory genes by integrating dynamic gene-gene interaction modeling with single-cell RNA sequencing (scRNA-seq) data. Rather than relying on DNA mutation calls, PICDGI infers functional driver activity from time-resolved expression patterns and latent regulatory influence among genes during tumor progression. Methodologically, PICDGI employs a time-varying state-space model with variational Bayesian inference and Markov Chain Monte Carlo (MCMC) sampling to estimate evolving gene interaction effects. The posterior distributions capture both the magnitude and uncertainty of each gene's inferred regulatory influence. From these, PICDGI derives a driver coefficient that quantifies the strength and reliability of each gene's contribution to progression-associated expression dynamics, enabling the prioritization of impactful regulators over neutral passengers. Applied to lung adenocarcinoma (LUAD) scRNA-seq data, PICDGI recovered known oncogenes and tumor suppressors and nominated novel candidate drivers, including JPH1 and CHEK1, which are implicated in calcium signaling, mitochondrial regulation, and DNA repair. These genes exhibit trajectory-aligned activity consistent with tumor evolution and immune-modulatory processes. Comparative analysis using Moran's I statistics in Monocle 3 showed that PICDGI-prioritized genes display stronger progression-associated dynamics than genes selected by spatial autocorrelation alone. We further validated PICDGI on an independent pediatric acute myeloid leukemia (AML) scRNA-seq cohort, where it consistently recovered known drivers and relapse-associated regulatory programs under fixed model parameters. By integrating interaction-informed dynamic modeling with single-cell resolution data, PICDGI provides a generalizable and biologically grounded framework for identifying rare and context-specific regulatory drivers of cancer progression, with broad applicability across tumor types. - Source: PubMed
Publication date: 2026/04/27
Atitey KomlanAnchang Benedict - Replication stress and resulting genome instability, a major driver of cancer progression, stem from perturbations of replication fork progression. The first defense against this stress is activation of "dormant" replication origins, which supports replication completion. To determine whether ATR, in itself, contributes to this compensation process, we submitted human cells to a range of low stresses sufficient to activate ATR, not CHK1. Using molecular combing, we developed a dose-response assay that quantifies compensation efficiencies, enabling accurate comparison of cells with different genotypes. Combined with Repli-seq and OK-seq, this assay revealed that ATR activation is key to compensation triggering. We next asked how TopBP1, the main ATR activator, impacts compensation. In stark contradiction to what would be expected from its checkpoint function, we found that TopBP1 represses compensation and acts downstream of ATR. Instead, the function of TopBP1 in replisome assembly, which remains unclear in mammalian cells where the protein is not essential, well-accounts for our results positing that TopBP1 locks dormant origins at the pre-initiation stage, an intermediate in the assembly process, and that ATR activation allows assembly to resume. TopBP1 engagement in the pre-initiation complex would thus serve as a switch linking replisome assembly to the stress response. - Source: PubMed
Koundrioukoff StéphaneAlary NathanKim Su-JungCollin ThibaultToffano AntoineMelendez-Garcia RodrigoWu XiaLiu YaqunGnan StefanoEl-Hilali SamiBrison OlivierRosselli FilippoChen Chun-LongDebatisse Michelle - 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