Human Polyclonal BMI1 Ab
- Known as:
- Human Polyclonal BMI1 Antibody
- Catalog number:
- a0211
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal BMI1
Related genes to: Human Polyclonal BMI1 Ab
- Gene:
- BMI1 NIH gene
- Name:
- BMI1 proto-oncogene, polycomb ring finger
- Previous symbol:
- PCGF4
- Synonyms:
- RNF51
- Chromosome:
- 10p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-05
- Date modifiied:
- 2016-10-05
Related products to: Human Polyclonal BMI1 Ab
Related articles to: Human Polyclonal BMI1 Ab
- - Source: PubMed
Publication date: 2026/07/03
Guo Bao-HongFeng YanZhang RongXu Li-HuaLi Man-ZhiKung Hsiang-FuSong Li-BingZeng Mu-Sheng - Primary ciliary dyskinesia (PCD) is a genetically heterogeneous disorder caused by defective motile cilia, resulting in impaired mucociliary clearance, chronic respiratory disease, laterality defects and subfertility. Currently, no disease-modifying treatments exist. Targeting PCD at its root cause requires emerging genetic therapies, such as small molecules, oligonucleotides, mRNA therapy, gene replacement and genome editing. With over 52 implicated genes and numerous patient-specific variants, there is a need for robust preclinical models to evaluate and accelerate these approaches. This review examines human preclinical models that recapitulate patient-specific genotypes and phenotypes while providing sufficient scalability for screening and detailed efficacy assessment. The models should also resolve knowledge gaps, including which cells need targeting and at what stage of differentiation. Air-liquid interface cultures of primary human airway epithelial cells or induced pluripotent stem cells (iPSCs) represent the current practice, alongside three-dimensional organoids, spheroids and lung-on-a-chip platforms. To overcome the limited proliferative capacity of primary cells, strategies include or transduction, conditional reprogramming with Rho-associated kinase (ROCK) inhibitors and feeder layers, and differentiation of iPSCs. Patient-derived and CRISPR-edited models have been developed for multiple PCD genes. Outcome measures to confirm efficacy of the therapy include high-speed video microscopy for quantifying ciliary beat pattern, transmission electron microscopy for ultrastructural assessment, mucociliary clearance assays and deep molecular phenotyping. There is a need for field-wide standardisation through consensus protocols, core outcome sets, minimum reporting criteria, quality benchmarks and regulatory alignment to facilitate accelerated translation of preclinical findings to clinical therapeutics. - Source: PubMed
Publication date: 2026/07/01
Ong Jonathan W YJackson Claire LArbi MarinaHart Stephen LMill PleasantinePaff TamaraRubbo BrunaShahaj EriominaShoemark AmeliaLucas Jane S - Nutritional biomarkers are linked to body composition changes, but limited evidence has studied how nutritional biomarkers relate to low muscle mass, excess adiposity, and both coexisting conditions across different physical activity levels. This study aims to investigate associations between low muscle mass, obesity, and low muscle mass with obesity and nutritional biomarkers across physical activity levels among U.S. adults across physical activity levels. - Source: PubMed
Publication date: 2026/06/19
Booranasuksakul UraipornSiervo MarioSinghato AlongkoteRueangsri NarisaSamrit TepparitSuriyawongpaisal WichukornPrasertsri Piyapong - Hepatoblastoma (HB), the most common pediatric liver cancer, exhibits marked variability in therapeutic response despite minimal genetic heterogeneity, implicating epigenetic regulation as a key driver of tumor behavior. Among these, polycomb repressor complexes (PRC) remain poorly explored as therapeutic targets. Integrative analysis of samples from patients with HB and public datasets identified BMI1, a core component of PRC1, as significantly upregulated, with high expression strongly associated with aggressive disease and poor survival. Functional screening of epigenetic inhibitors across 15 HB cell lines revealed BMI1 inhibition as the most effective therapeutic strategy, with strong concordance between in vitro predictions and in vivo responses in patient-derived xenograft (PDX) models. The BMI1 inhibitor PTC596 demonstrated the highest potency, consistently suppressing tumor growth across models. Mechanistically, PTC596 induced BMI1 degradation, reduced histone H2A ubiquitination, impaired microtubule dynamics, and restored intrinsic apoptosis by shifting the BCL2-BAX balance, leading to caspase-3/7 activation. Transcriptomic profiling confirmed apoptosis as the most significantly enriched pathway. In vivo, PTC596 markedly reduced tumor burden and proliferation while inducing pro-apoptotic signaling, without detectable toxicity. Together, these findings establish BMI1 as a critical oncogenic dependency in HB, demonstrate the value of robust preclinical tumor modeling for therapeutic validation, and identify PTC596 as a promising, mechanism-based treatment strategy. - Source: PubMed
Publication date: 2026/06/10
Demir SalihBentrop Marie FriederikeHotes AlinaSchmid TanjaIndersie EmilieBranchereau SophieVokuhl ChristianHäberle BeateSchmid IreneCairo StefanoKappler Roland - Melanoma differentiation associated gene-9 (MDA-9), also known as Syntenin-1 or SDCBP, exhibits elevated expression in multiple cancers, promoting invasion, migration, and tumor cell survival. The TCGA database reveals high MDA-9 expression in late-stage HPV (-) HNSCC tissues, which associates with poor patient survival. Moreover, bioinformatics analyses support a potential role of MDA-9 in promoting cancer stemness in HNSCC tissues. We characterized the functional role of MDA-9 in HNSCC tumorigenesis, particularly in relation to cancer stem cell maintenance. Knockdown of MDA-9 suppresses BMI1, a functional cancer stem cell marker in HNSCC, and the self-renewal of cultured HNSCC cells. Mechanistically, MDA-9 controls expression of BMI1 through NF-κB p65. Targeting MDA-9 with a specific small molecule pharmacological inhibitor, IVMT-Rx-4, inhibits HNSCC growth and metastasis in a HNSCC xenograft mouse model. In vivo lineage tracing reveals that IVMT-Rx-4 potently inhibits self-renewal and tumorigenicity of Bmi1 cancer stem cells in a spontaneous model of HNSCC. Additionally, IVMT-Rx-4 significantly improves treatment with cisplatin by eliminating cisplatin-enriched Bmi1 cancer stem cells, thereby overcoming cisplatin resistance. Taken together, our results demonstrate that targeting MDA-9 with IVMT-Rx-4 is an effective strategy for treating HNSCC by eliminating cancer stem cells, and IVMT-Rx-4 is a promising chemical entity that may be amenable for developing an effective therapy for HNSCC. - Source: PubMed
Publication date: 2026/06/24
Rilee Grace JZaman Shadid UManupati KanakarajuMa ZhikunHoyle Rosalie GBacolod Manny DLopresti Marion QBrown Anne MDas Swadesh KFisher Paul BLi Jiong