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
- : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
Rutecki SzymonKrawiec AdriannaLeśniewska-Bocianowska AgnieszkaMatuszewska JuliaNaumowicz ErykSzubert SebastianKsiążek KrzysztofMikuła-Pietrasik Justyna - Embryonic genome activation (EGA) marks the onset of transcriptional autonomy in the developing embryo, a process that is still not well characterized in pigs. Emerging evidence suggests that chromatin remodeling events during EGA and DNA damage response (DDR) may share regulatory mechanisms. In mouse and human embryos, the double homeobox (Dux) transcription factor acts as a pioneer regulator of EGA and may also contribute to DDR. However, the role of the porcine orthologue, DUXA, in early embryogenesis is not well understood. In this study, we show that DUXA mRNA is highly expressed in porcine embryos at the EGA stage, with levels declining at post-EGA and blastocyst stages. Attenuation of DUXA mRNA did not impair blastocyst formation or lineage allocation to the inner cell mass and trophectoderm. Unexpectedly, DUXA mRNA attenuation increased total cell number in both blastocysts and embryos arrested prior to blastocoel formation. DUXA mRNA attenuation decreased mRNA levels of EGA-related (EIF1AX), cell cycle checkpoint (CHEK1), and DDR-associated genes (BRCA1), and was accompanied by increased DNA damage at late/post-EGA stages. Induced DNA damage upregulated transcripts of EGA-related (DPPA2, KDM5B, EIF2A) and DDR-associated genes (P53, RAD51) on day 4 of development. Interestingly, DNA damage induction in DUXA mRNA-attenuated embryos abrogated the impact on cell proliferation and enhanced transcript levels of checkpoint (CHEK1 and XIAP) and DDR (P53, KU-70 and KU-80) genes. These findings suggest that while DUXA is not essential for parthenogenetic blastocyst formation in pigs, it may play a regulatory role in embryonic cell proliferation, checkpoint activation, and the DNA damage response. - Source: PubMed
Publication date: 2026/05/12
Facioli Fernanda LuizaGlanzner Werner GiehlGutierrez Karinade Macedo Mariana Priottoda Silva ZigomarGuay VanessaCurrin Luke GeorgeCarrillo Herrera María ElenaBordignon Vilceu - Olaparib is registered for use in ovarian, breast, pancreatic and prostate cancers with a BRCA1/2 mutation and/or mutations in other homologous recombination deficiency (HRD) genes. HRD gene mutations are also found in other cancer types, and these cancers may also benefit from olaparib therapy. We aimed to evaluate the efficacy of olaparib in advanced cancers harboring a (likely) pathogenic germline or somatic mutation in a gene involved in homologous recombination (HR). - Source: PubMed
Publication date: 2026/05/08
Joris SDenys HCollignon JRasschaert Mde Roodenbeke D TDuhoux F PCanon J LTejpar SMebis JDecoster LAftimos PDe Grève J - Glioblastoma harbors frequent alterations in the retinoblastoma (RB1) pathway, providing a genetic rationale for therapeutic targeting with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors. The NOA-20 trial did not reveal a progression-free survival benefit of CDK4/6 inhibition plus radiation therapy in newly diagnosed, MGMT-unmethylated glioblastoma. In fact, CDK4/6 inhibitor monotherapy has not demonstrated efficacy in solid tumors. We aimed at discovering response modulators to CDK4/6 inhibition, paving the way for rational combination therapies. - Source: PubMed
Publication date: 2026/05/04
Surender SurenderHaeusser Lara AnninaKuhlburger LaurenceTsiami FoteiniDogan Nihal OlcayMaise LouiseNahnsen SvenBeck SusanneMerk Daniel JosefTabatabai Ghazaleh - 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