CDC45L Blocking Peptide
- Known as:
- CDC45L Blocking Peptide
- Catalog number:
- 33r-9861
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CDC45L Blocking Peptide
Related genes to: CDC45L Blocking Peptide
- Gene:
- CDC45 NIH gene
- Name:
- cell division cycle 45
- Previous symbol:
- CDC45L2, CDC45L
- Synonyms:
- -
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-08
- Date modifiied:
- 2014-11-19
Related products to: CDC45L Blocking Peptide
Related articles to: CDC45L Blocking Peptide
- Mammalian cells frequently enter mitosis before DNA replication has finished, necessitating the rapid processing of unreplicated loci to facilitate chromosome segregation. The TRAIP ubiquitin ligase induces replisome disassembly during mitosis, triggering the cleavage of DNA replication forks. Until now, the mechanisms that regulate TRAIP and process cleaved DNA replication forks were unclear. Here we show that the TTF2 ATPase is a new type of phospho-receptor that binds a conserved phosphorylation site on TRAIP during mitosis. TTF2 couples phosphorylated TRAIP to DNA polymerase epsilon (Pol ε) in the replisome, leading TRAIP to ubiquitylate the CDC45-MCM-GINS (CMG) helicase. This triggers mitotic replisome disassembly, and a repair pathway that produces sister-chromatid exchanges, supporting a model for how fork cleavage promotes the segregation of under-replicated loci in mammalian cells. - Source: PubMed
Publication date: 2026/07/02
Fujisawa RyoLabib Karim P M - Breast cancer remains the most common malignancy in women, and substantial heterogeneity in treatment response and prognosis persists despite multimodal therapies. The acidic tumor microenvironment (TME), driven by metabolic reprogramming and lactate accumulation, is recognized as a key driver of tumor adaptation, immune evasion, and therapeutic resistance. However, the genomic and transcriptomic patterns of acidosis tolerance in human breast cancer, and their implications for subtype stratification and targeted therapy, remain poorly understood. - Source: PubMed
Publication date: 2026/06/29
Li YiWu DihengShi ZhenyiLuo QianDeng WenyueLiu QinwenLu AipingChen WeiguoQin GenggengGuan Daogang - Inhibitors of ATR, a central kinase controlling DNA replication origin firing and cellular checkpoints, are undergoing clinical trials, yet mechanisms underpinning sensitivity to ATR inhibitors (ATRi) and patient stratification biomarkers are lacking. Here, we perform in parallel, proteomics, transcriptomics and functional analyses and demonstrate that sensitive cancer cell lines have higher expression of DNA replication initiation factors, and exhibit higher origin firing, increased pan-nuclear γH2AX signals and cell death upon ATRi treatment. ATRi sensitivity is causally associated with origin firing rates, since we could modulate ATRi sensitivity by either up- or down-regulating origin firing capacity using CDC7 inhibition, CDK2 inhibition or CDC45 overexpression in both breast and colorectal cancer cells. High expression of replication initiation factors predicts ATRi sensitivity across cell lines from multiple cancer types and acute myeloid leukemia patient samples. This study reveals a contribution of lethal origin firing capacity to ATR sensitivity, providing key steps towards developing a multimodal clinically applicable biomarker. - Source: PubMed
Publication date: 2026/06/19
Lumeau APfuderer P LScarth J AManiati EGuscott M AShaikh NCopley F BGerdes HDe Angelis SAlard E LWang JCutillas P RMardakheh F KBoemo M AForment J VMcClelland S E - When cells enter S phase, bidirectional DNA replication is initiated through the kinase-regulated recruitment of three activators (Cdc45, GINS and Pol ε) to a duplex-DNA-loaded double hexamer of minichromosome maintenance (MCM) ATPases. Together, these proteins form two CMGE helicases that establish divergent replication forks as they become separated. Here, to gain an understanding of CMGE biogenesis, we reconstituted the pre-initiation complex with purified yeast proteins. The cryo-electron-microscopy structure shows a set of firing factors caught in the act of assembling two symmetrical CMGEs. We show how stepwise complex formation reshapes MCM in preparation for DNA opening, and we explain how ATP promotes firing-factor ejection and CMGE maturation. We find that although Sld2 facilitates the recruitment of GINS to MCM, as expected, it also aids the efficient separation of the CMGE dimer, and is essential for the ejection of the lagging strand from MCM. These findings have direct implications for our understanding of the metazoan Sld2 orthologue, RECQL4, and point to a replication-fork establishment mechanism that is conserved across eukaryotes. - Source: PubMed
Publication date: 2026/06/17
Pühringer ThomasCanal BertaPalm GiacomoButryn AgataCouves Emma CWillhoft OliverLewis Jacob SDiffley John F XCosta Alessandro - The leg muscles of poultry are an important source of high-quality protein and key trace elements. Most of the research on muscle development are focused on the embryonic or growth stage, there is relatively little research on the muscle development of chicken from embryonic stage to growth stages. Therefore, in this study, transcriptome sequencing was performed on leg muscle samples from female Huanglang chickens across embryonic (E13, E17) to growth stages (D1, D14, D35). A total of 7,691 differentially expressed genes (DEGs) were identified by comparison in pairs of the ten groups, and the highest number of DEGs was observed between E13 and D35, with 4,645 DEGs. Time-series expression analysis using STEM revealed three distinct expression clusters: cluster I (2,582 genes, downregulated genes), cluster II (1,666 genes, upregulated genes), and cluster III (614 genes, transient upregulation peaking at D1). GO and KEGG enrichment analyses showed that the DEGs were enriched in pathways such as cell cycle and DNA replication (cluster I), metabolic and muscle structure-related pathways (cluster II), oxidative phosphorylation and mitochondrial function (cluster III). Protein-protein interaction network analysis identified hub genes, including CDC45/MCM complex members in cluster I, mitochondrial genes such as CYTB and ND1 in cluster II, and oxidative phosphorylation genes including NDUFS3 and COX5A in cluster III. Transcription factor prediction highlighted KDM5A, KDM5B, PHF8, and SAP30 as key regulators. The RT-qPCR results of seven genes (ACTN2, PDK4, MYOG, MYOD1, MYH1F, MYH1B, and MYF6) were consistent with the RNA sequencing (RNA-seq) analysis. This study is the first to systematically analyzed the leg muscle development mechanisms of local chicken breeds from embryonic stage to early growth stage. It provides a comprehensive transcriptomic resource for understanding leg muscle development in chickens. - Source: PubMed
Publication date: 2026/05/28
Liu XuWang ZihanChen TingLiang HongniYang CanYang HaiDeng Yuying