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
- This study aimed to investigate the distinct subtypes of anoikis in hepatocellular carcinoma (HCC) and their underlying molecular mechanisms, and to construct a prognostic risk model. The gene expression profiles of HCC were downloaded from the cancer genome atlas and gene expression omnibus database, while anoikis-related genes were obtained from the GeneCards database. Unsupervised clustering algorithms were applied based on the expression of differentially expressed anoikis genes to identify related subtypes. Survival curves were used to analyze the differences in survival between subtypes, and the enrichment pathways and immune microenvironment differences were explored. Limma analysis, Cox proportional hazards regression analysis, and Least absolute shrinkage and selection operator regression algorithms were utilized to identify genes affecting the prognosis of subtypes and to construct a prognostic model, while also classifying high and low-risk groups for immune correlation analysis. The study identified 2 subtypes, C1 and C2, which showed significant differences in survival probability, enriched pathways, and immune microenvironment. SFN, BUB1, BSG, and HMOX1 were identified as prognostic genes, and a prognostic model was successfully constructed. There were significant differences in prognosis, expression of prognostic genes, and immune microenvironment between the high-risk and low-risk groups. The identification of different subtypes of anoikis in HCC and the construction of a prognostic model provide new insights and directions for the treatment and prognosis research of HCC. - Source: PubMed
Zhang XifengChen FeihuaQiu RongxianYe XiangyangHu Zhenting - Phaeochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumours with limited treatment options in the metastatic setting. We performed integrative transcriptomic analyses of TCGA and COMETE datasets and identified BUB1, a mitotic checkpoint kinase and prototypical non-oncogene addiction (NOA) factor, as significantly upregulated in metastatic PPGLs. We validated BUB1 overexpression in primary tumour tissues using RT-qPCR and subsequently conducted functional studies in the human phaeochromocytoma-derived hPheo1 cell line. Genetic silencing of BUB1 or its pharmacological inhibition with BAY1816032 significantly reduced cell viability, colony formation, migration, and invasion. Both interventions also decreased phosphorylation of histone H2A at threonine 120, a direct downstream target of BUB1 kinase activity. In migration and invasion assays, BUB1 inhibition impaired motility and reduced expression of the epithelial-to-mesenchymal transition (EMT) markers N-cadherin and vimentin. These findings provide the first demonstration of BUB1 overexpression in metastatic PPGL tissues. Preclinical evidence suggests that hPheo1 cells depend on BUB1 for growth, genome stability, and invasive behaviour. These findings nominate BUB1 as a candidate vulnerability and putative biomarker, warranting validation in larger, multi-institutional cohorts. - Source: PubMed
Publication date: 2026/04/21
Ahmadi MarziehsadatZargar Seyed JalalAlkaissi HussamGhayee Hans KPacak KarelJandaghi PouriaAuld Daniel - The murine C1498 cell line is one of the most widely used syngeneic models to investigate acute myeloid leukemia (AML) pathogenesis, tumor-host interactions and therapeutic responses. However, in the absence of a comprehensive molecular characterization it remains impossible to reliably associate genetic lesions with disease phenotype, drug sensitivity or resistance. Here, we provide an integrated genomic and functional analysis combining whole genome and whole transcriptome sequencing (WGS and WTS), multicolor fluorescent in situ hybridization (M-FISH) and drug sensitivity assays. WGS identified 2,007 coding variants absent from population databases, including functionally relevant alterations in AML-related genes. These comprised deleterious or likely pathogenic variants in , and (murine ortholog of the human gene), a splice-site mutation in and truncating variants in and . Structural variant analysis revealed 1,767 events, including deletions of , ,,,, and cohesin genes, and tandem duplication. Copy number variant profiling detected ten tumor-specific alterations, including amplifications of and , the latter linked to aggressive cancer phenotypes. Variants integration uncovered biallelic disruption of , double-hit events affecting additional tumor suppressors (mutation and deletion: , ) and oncogenes (mutation and amplification: , , ,). Functionally, C1498 demonstrated in vitro a dose- and time-dependent response to venetoclax/azacitidine consistent with resistance, in line with the presence of altered and recent prognostic AML signatures. This comprehensive molecular framework establishes C1498 as a genetically defined AML model and provides a valuable resource to inform biomarker-driven preclinical studies and translational research aimed at overcoming venetoclax/azacitidine resistance. - Source: PubMed
Publication date: 2026/04/10
Ghetti MartinaDe Santis IlariaTolomeo DoronRuggieri FrancescaBracci ChiaraBochicchio Maria TeresaPaganelli MatteoFerrari AnnaSangaletti SabinaStorlazzi Clelia TizianaSimonetti Giorgia - - Source: PubMed
Publication date: 2026/04/10
- HPV types 16 and 18 are associated with 70% of invasive cervical cancers. Between these two types of HPV, HPV type 16 is more commonly found in cervical cancer patients, whereas HPV type 18 is less frequently reported. Currently, the molecular mechanism underlying the increased cancer risk in HPV type 16, compared to HPV type 18, has not yet been fully elucidated. - Source: PubMed
Publication date: 2026/04/01
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