BUB1 & APC Protein Protein Interaction Antibody Pair
- Known as:
- BUB1 & Antigen presenting cellular Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0053
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BUB1 & APC Protein Interaction Antibody Pair
Related genes to: BUB1 & APC Protein Protein Interaction Antibody Pair
- Gene:
- BUB1 NIH gene
- Name:
- BUB1 mitotic checkpoint serine/threonine kinase
- Previous symbol:
- BUB1L
- Synonyms:
- hBUB1, BUB1A
- Chromosome:
- 2q13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-18
- Date modifiied:
- 2017-07-14
Related products to: BUB1 & APC Protein Protein Interaction Antibody Pair
Related articles to: BUB1 & APC Protein Protein Interaction Antibody Pair
- Autism spectrum disorder (ASD) can present with either an essential or a complex phenotype. The aim of this study was to compare clinical characteristics and the diagnostic yield of copy number variations (CNVs) in essential and complex phenotypes, and to evaluate risk factors. A total of 163 Turkish children (126 boys, 37 girls) who met the DSM-5 diagnostic criteria for ASD were evaluated. Chromosomal microarray analysis was performed. Among the patients, 21.5% had a complex phenotype and 78.5% had an essential phenotype. Overall, 13.7% of the patients had a developmental/intelligence quotient (DQ/IQ) below 50, most of whom had a complex phenotype. In contrast, 15.3% of the patients had a DQ/IQ of 70 or higher, all of whom had an essential phenotype. The frequency of verbal individuals was 30.5% and did not differ between the two phenotypes. Pathogenic CNVs were identified in 7.4%; 17.1% of the complex group and 4.7% of the essential group. CNVs of uncertain significance that were potentially causal because they included an ASD-associated gene were present in 12.3% of individuals. CNV positivity was significantly higher in individuals with an IQ below 50; interestingly, it was similar between the verbal and non-verbal groups. Besides ultra-rare CNVs, recurrent CNVs associated with ASD were identified. A novel pathogenic CNV was identified at 2q13.33, including and , both of which are expressed in the brain and are potentially associated with ASD. Advanced parental age and preterm birth were identified as possible risk factors. Deep phenotyping is important for the management of both essential and complex phenotypes and allows the identification of patients with a higher probability of having CNVs. Reporting novel or rare CNVs contributes to clarifying the pathogenesis of ASD. - Source: PubMed
Publication date: 2026/08/30
Tüysüz BeyhanÇifçi Sunamak EvrimDurcan GizemÖztürk BirolUludağ Alkaya DilekÇulpan Hazal CansuKorkmaz Mehmet BarışDoğangün BurakKıykım Ertuğrul - Solid tumors including glioblastoma (GBM), lung cancer (LC), and triple-negative breast cancer (TNBC) exhibit marked radioresistance driven by dysregulated cell-cycle control and genomic instability. Although CDK4/6 inhibitors suppress tumor proliferation, their radiosensitizing capacity is limited by persistent DNA repair. BUB1, a mitotic checkpoint kinase overexpressed in aggressive cancers, has emerged as a regulator of DNA damage signaling. We tested whether co-targeting BUB1 and CDK4/6 enhances radiosensitivity across solid tumors. GBM, LC, and TNBC cell lines were treated with BUB1 inhibitor BAY1816032, CDK4/6 inhibitors ribociclib and abemaciclib, and radiation. Proliferation, clonogenic survival, immunoblotting, and combination index analyses assessed cytotoxicity and synergy. CDK4/6-resistant models were generated to examine resistance. In vivo efficacy was evaluated using SUM159 xenografts. DNA damage and homologous recombination repair were measured by gH2AX, RAD51, RPA, BrdU foci and comet assay. The resection branchpoint was assessed by phospho-RPA, with ATR inhibition and BLM or EXO1 depletion testing resection dependence. BUB1 inhibition increased cytotoxicity in vitro and improved therapeutic response in vivo. Combined BUB1 and CDK4/6 inhibition showed strong synergy (C.I. < 1) and enhanced radiosensitization in RB+ models. CDK4/6-resistant cells displayed increased BUB1 expression, and BUB1 inhibition partially restored sensitivity. Mechanistically, dual inhibition intensified homologous recombination defects, marked by persistent gH2AX and altered RAD51, RPA, and BrdU dynamics, consistent with sustained single stranded DNA and impaired HR repair. Persistent RPA32 Ser33 phosphorylation reflects ATR-dependent resection that requires BLM and EXO1 at later stages, supporting sustained resection and unresolved repair leading to increased cell death. Dual inhibition of BUB1 and CDK4/6 represents a promising therapeutic strategy for enhancing radiosensitivity in GBM, lung cancer, and TNBC, particularly in Rb-intact settings. - Source: PubMed
Publication date: 2026/08/29
Thoidingjam ShivaniSriramulu SushmithaHaider Muratoglu AsyaHede-Sakhardande RheaGhosh SunitaDavis Anthony JBrown Stephen LSiddiqui FarzanMovsas BenjaminSpeers CoreyNyati Shyam - Intrauterine adhesion (IUA) represents a prevalent cause of persistent infertility and continues to be a significant unresolved challenge in reproductive medicine. However, its full pathogenic mechanisms remain incompletely elucidated. We retrieved endometrial RNA-sequencing data from IUA patients and normal controls in the Gene Expression Omnibus (GEO) database, and screened 586 differentially expressed genes (DEGs) in the endometrium of IUA patients using the R package limma. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) revealed activation of immune-related pathways, including chronic inflammatory response, complement activation, and complement and coagulation cascades in IUA. Further single-sample gene set enrichment analysis (ssGSEA)-based relative immune cell enrichment analysis revealed decreased enrichment scores of activated CD4 T cells and type 2 T helper cells, alongside increased enrichment scores of effector memory CD8 T cells, macrophages, mast cells, natural killer cells, and T follicular helper cells in IUA patients, indicating their potential involvement in IUA pathogenesis. A protein-protein interaction (PPI) network was constructed, identifying 10 hub genes associated with IUA: , , , , , , , , , and . The expression patterns of these genes were further validated in two independent external IUA cohorts, supporting a potential correlative link between these genes and IUA pathogenesis. Our findings provide exploratory insights and potential candidate molecules for subsequent mechanistic studies of IUA onset and progression. - Source: PubMed
Publication date: 2026/09/20
Feng XueYu Lili - While CAR-T cell therapy has transformed outcomes in B-cell malignancies, most genomic insights originate from clinical trials. There is a paucity of data describing molecular changes during CAR-T manufacturing in real-world practice, particularly for non-US CAR constructs. - Source: PubMed
Publication date: 2026/09/03
Das NupurMehta PrashantGupta KusumKatharia RahulPabbi SwatiMishra PravasMorya Soni - Human-induced pluripotent stem cells (iPSCs) hold considerable potential for generating motor neurons (MNs), offering new avenues for disease modeling and regenerative medicine. To elucidate the molecular mechanisms underlying iPSC differentiation into MNs, we conducted an integrated bioinformatics analysis of transcriptomic data from the mature Day 28 stage of a publicly available 28-day iPSC differentiation dataset Protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape, while CytoHubba identified 15 hub genes, including BUB1, TOP2A, AURKB, CCNA2, and TP53, which are primarily associated with cell cycle regulation, mitotic progression, and genomic stability. Gene Ontology (GO) enrichment analysis identified biological functions related to chromosomal organization, cytoskeletal remodeling, metabolic activity, and translational regulation, whereas Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted cell cycle, DNA replication, cellular senescence, p53 signaling, and oocyte meiosis. CytoCluster analysis identified distinct subnetwork modules linked to neuronal differentiation. Promoter motif analysis via MEME uncovered conserved transcription factor binding sites, whereas miRNA-mRNA interaction prediction using the psRNATarget database identified 5316 potential regulatory pairs that may fine-tune gene expression during MN maturation. Codon usage analysis of 163 genes indicated moderate to high translational optimization, likely influenced by both mutational bias and selective codon preferences, with GC3 content strongly affecting codon choice. These patterns suggest potential mechanisms that may promote efficient protein synthesis during MN differentiation; however, experimental validation is required. This systems-level bioinformatics framework integrates multiple computational analyses to characterize transcriptional, post-transcriptional, and translational regulatory mechanisms associated with human MN differentiation. However, as these results are derived from bioinformatics analyses, they warrant further experimental validation and have the potential to advance our understanding of the molecular interactions and signaling pathways that regulate MN differentiation and maturation. These findings provide a computational framework for exploring regulatory mechanisms of motor neuron differentiation and prioritizing candidate genes for future experimental validation. - Source: PubMed
Publication date: 2026/08/12
Sadeghi MaryamHadifar ShimaGhorbani Abozar