BUB1
- Known as:
- BUB1
- Catalog number:
- 002736A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BUB1
Ask about this productRelated genes to: BUB1
- 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
Related articles to: BUB1
- 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 - Epigenetic regulation is essential for development and adaptation across eukaryotes. However, a comprehensive overview of the molecular framework of chromatin-mediated regulation, particularly in non-model organisms, is lacking. Here, we present a systematic proteomic characterization of the chromatin domains in P. falciparum, an ancient human pathogen with a unique genome composition and epigenetic blueprint. We adapted and employed three proximity-labeling approaches to provide a high-confidence and comprehensive proteome of heterochromatin, euchromatin, and (peri)centromeric chromatin comprising 214 proteins, including both expected and new chromatin components. Characterization of 20 proteins validated our approach and uncovered (1) a protein influencing parasite transmission, (2) complexes relevant for histone variant exchange and chromatin-RNA interactions, and (3) the so-far believed-to-be-absent spindle assembly checkpoint and the corresponding Bub1-like kinase. This study hence offers a reference proteome of the chromatin domains and a resource to uncover novel chromatin biology. - Source: PubMed
Publication date: 2026/08/17
Ramón-Zamorano GalaMainye SheilaKimmel Jessicade Krijger IngeKanyal AbhishekHoráčková VendulaGockel Jonasvan den Broek MartijnGuo YangyangPetter MichaelaGraser MaxGuillén-Samander AndrésVermeulen MichielSpielmann TobiasBártfai Richárd - Cervical cancer (CC) is the fourth most common cancer in women worldwide. New therapeutic targets are urgently needed considering the inadequacy of current treatments. In this study, we investigated the role of budding uninhibited by benzimidazoles 1 (BUB1) in CC and identified a dual mechanism through which BUB1 promotes tumor progression. BUB1 interacted with α-actinin 1 (ACTN1) and regulated its subcellular distribution: BUB1 maintained ACTN1 at focal adhesions to sustain AKT activation, while facilitating ACTN1-positive comet tail-propelled autophagosome trafficking toward lysosomes. Autophagosome accumulation elevated reactive oxygen species (ROS), which causally contributed to apoptosis, as demonstrated by NAC rescue experiments. Kinase-dead BUB1 failed to rescue these phenotypes. Furthermore, kinase inhibitor of BUB1, 2OH-BNPP1, phenocopied the ACTN1 intracellular localization of BUB1 knockdown, confirming the requirement for BUB1 kinase activity. 2OH-BNPP1 treatment significantly reduced the growth of subcutaneous xenograft tumors, highlighting the potential of BUB1 as a promising therapeutic target for CC. - Source: PubMed
Publication date: 2026/08/06
Sun YuZhang JunhuaGuo LingyuZhang JiaxinChen QianJia ZongyangLiu XiaoliSun YueChi ShuqiCui BaoxiaZhang YouzhongHan Sai - High-linear energy transfer (LET) radiation such as carbon ions exhibits greater biological effectiveness than conventional low-LET X-rays, but the transcriptional mechanisms underlying this advantage remain incompletely understood. We hypothesized that high-LET radiation induces a qualitatively different transcriptional response rather than simply amplifying low-LET signaling. - Source: PubMed
Publication date: 2026/07/14
Nisar HasanSerçin ÖzdemirhanHellweg Christine E