Ask about this productRelated genes to: BUB1B antibody
- Gene:
- BUB1B NIH gene
- Name:
- BUB1 mitotic checkpoint serine/threonine kinase B
- Previous symbol:
- -
- Synonyms:
- BUBR1, MAD3L, Bub1A, SSK1
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2019-04-23
Related products to: BUB1B antibody
Related articles to: BUB1B antibody
- Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha - Hub genes associated with non-small cell lung cancer (NSCLC) were identified through bioinformatics screening. In vitro experiments analyzed the potential mechanisms by which these genes regulate tumor malignant phenotypes and macrophage polarization. Differentially expressed genes were identified from The Cancer Genome Atlas (TCGA)-NSCLC and GSE32175 datasets, followed by protein-protein interaction (PPI) network analysis to screen hub genes. The effects of MYB Proto-Oncogene Like 2 (MYBL2) on NSCLC progression and macrophage polarization were evaluated using in vitro models. The regulatory relationship between MYBL2 and C-C motif chemokine ligand 2 (CCL2) was investigated by Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays, and rescue experiments were performed to validate the role of the MYBL2-CCL2 axis. Bioinformatics screening identified BUB1B, CDCA2 and MYBL2 as key hub genes with high expression in NSCLC, among which MYBL2 was significantly upregulated in NSCLC cells. Functional experiments confirmed that MYBL2 silencing markedly inhibited the malignant proliferation, migration and invasion of NSCLC cells. Tumor cell MYBL2 knockdown effectively reversed M2-like polarization and promoted M1-like polarization in the co-culture system. Mechanistically, MYBL2 directly bound to the CCL2 promoter region to enhance CCL2 transcriptional activity and upregulate CCL2 expression in NSCLC cells. Exogenous CCL2 supplementation significantly rescued the inhibitory effect of MYBL2 knockdown on macrophage M2-like polarization, verifying the mediating role of CCL2 in this regulatory axis. MYBL2 is strongly expressed in NSCLC cells and is associated with enhanced malignant phenotypes. It may affect macrophage M2-like polarization by upregulating CCL2, thus participating in NSCLC immune microenvironment remodeling. - Source: PubMed
Publication date: 2026/09/10
Sun QiongMeng JingMcGowan RochelleHodge BelindaShan DanielMiller NicolasShi Weiwei - In the developing human placenta, three subtypes of trophoblast cells, cytotrophoblasts (CTBs), extravillous trophoblasts (EVTs), and syncytiotrophoblasts (STBs), mediate critical functions essential for a successful pregnancy. CTBs constitute the stem/progenitor compartment and differentiate into STBs and EVTs within the floating and anchoring villi, respectively. STBs establish the maternal-fetal exchange interface and secrete human chorionic gonadotropin (hCG), a hormone vital for the maintenance of early pregnancy. EVTs anchor the maternal endometrium and invade the uterine tissue to remodel maternal cells, supporting implantation and progression of pregnancy. In this study, we used human trophoblast stem cells (hTSCs) as a model system and performed quantitative, label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS) to profile the proteome and phosphoproteome in TSC stem state (analogous to undifferentiated CTBs) and following their differentiation to STBs and EVTs. Through a multiomics approach, we integrated our proteomics data with global gene expression profiles to correlate cell-type specific gene and protein expression during human trophoblast development. We also identified global phosphoproteome and analyzed kinases that are specifically active in hTSC stem state, as well as in differentiated STBs and EVTs. We experimentally validated specific kinases, such as BUB1B, PAK6, PKYMT1, and TNIK, that are essential for maintaining the hTSC stem-state. Additionally, atypical protein kinase C isoforms PKCζ are essential for STB development, whereas PTK2B, SRC, TRIO, and LYN are important for EVT development. Our findings highlight key kinases uniquely required for specific stages of trophoblast development during human placentation and suggest that pharmacological inhibition of these kinases could negatively impact the placentation process during pregnancy. - Source: PubMed
Kumar RajnishDasgupta PurbasaRay SomaPaul Soumen - Small cell lung cancer (SCLC) is characterized by pervasive chromosomal instability (CIN) and remains largely refractory to targeted therapies. KIF18A, a motor protein that regulates chromosome alignment during mitosis, has emerged as a selective dependency in CIN-high tumors. Whether this dependency extends to SCLC, a prototypical CIN-high cancer, has not been established, and biomarkers predicting response to KIF18A inhibition, currently in clinical trials, are lacking. We integrated analyses of patient tumor datasets, neuroendocrine (NE) and non-NE SCLC cell lines, and functional perturbation models to define the determinants of response to KIF18A inhibition. CIN metrics, transcriptional programs, mitotic dynamics, and spindle assembly checkpoint (SAC) function were assessed using genomic profiling, live-cell imaging, genetic perturbation, and pharmacologic inhibition. KIF18A expression was elevated in SCLC tumors and correlated with CIN-associated transcriptional programs, proliferative markers, and NE status; however, these features did not predict sensitivity to KIF18A inhibition. Instead, response was determined by the functional integrity of the SAC. SAC-proficient SCLC cells underwent sustained mitotic arrest followed by apoptotic cell death upon KIF18A inhibition, whereas SAC-defective cells failed to maintain checkpoint activation and survived. Mechanistically, resistant cells exhibited impaired kinetochore recruitment of core SAC components, including MAD1L1 (MAD1) and BUB1B (BUBR1). Importantly, transient induction of acute CIN through TTK (MPS1) inhibition partially restored sensitivity to KIF18A inhibition in resistant models. This study provides the first mechanistic characterization of KIF18A dependency in SCLC, identifying SAC competency as the primary determinant of response. These findings establish a biologically informed framework for patient stratification and rational combination strategies. - Source: PubMed
Tabe ChioriKumar RajeshHuang YueKruhlak Michael JSharma Ajit KumarShrestha Roshan LThomas Anish - Preoperative differentiation between uterine mesenchymal tumors and benign uterine fibroids remains challenging in postmenopausal women. This study aimed to develop an exploratory risk-stratification model for uterine mesenchymal tumors and to characterize complementary molecular features of uterine leiomyosarcoma using a public transcriptomic dataset. A retrospective case-control study was conducted in postmenopausal patients with uterine masses who underwent surgery between 2011 and 2021. A total of 23 uterine mesenchymal tumor cases and 92 frequency-matched fibroid controls were included. Clinical variables were analyzed using univariable and multivariable logistic regression to develop an exploratory risk-stratification model. Model performance was evaluated using ROC analysis, calibration analysis, decision curve analysis, and confusion matrix assessment. Exploratory transcriptomic analysis was performed using the GEO dataset GSE64763 to characterize molecular differences between uterine leiomyosarcoma and fibroid tissues. Pelvic pressure, abnormal uterine bleeding, and tumor diameter were independently associated with uterine mesenchymal tumors. The model achieved an apparent AUC of 0.859 and an optimism-corrected AUC of 0.846 after 1000 bootstrap resamples. Exploratory transcriptomic analysis revealed distinct expression patterns and upregulation of proliferation-associated genes, including CCNB1, BUB1B, PRC1, TOP2A, and FOXM1, with enrichment of cell cycle-related pathways. An exploratory model based on routinely available preoperative variables demonstrated preliminary discriminatory ability within the development cohort. Independent external validation in representative prospective cohorts is required before any assessment of clinical utility. - Source: PubMed
Publication date: 2026/07/31
Wan XiaojieZhang TaoLi JingyiSong ZhiminRuan FeiLuo Jie