BMI1 polyclonal antibody
- Known as:
- BMI1 pab (anti-)
- Catalog number:
- PAB9982
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BMI1 polyclonal antibody
Related genes to: BMI1 polyclonal antibody
- 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: BMI1 polyclonal antibody
Related articles to: BMI1 polyclonal antibody
- Mechanical forces shape the growth and regeneration of mineralized tissues such as bones and teeth, yet how these tissues adapt to sustained mechanical stress remains poorly understood. Here, using mouse incisor models with varying degrees of loading, we identified that the histone demethylase KDM6B is a critical epigenetic regulator that preserves mineralized tissue homeostasis by protecting progenitor transit-amplifying cells from mechanical stress-induced apoptosis. Loss of Kdm6b impairs this balance by enhancing PIEZO1-dependent mechanotransduction, leading to excessive Ca influx and apoptosis in transit-amplifying cells. Mechanistically, Kdm6b deficiency increases H3K27me3 at the Bmi1 promoter, silencing its expression and derepressing Piezo1 expression. Importantly, Piezo1 haploinsufficiency in Kdm6b-deficient mice restores Ca influx restriction, rescuing transit-amplifying cell defects and tissue homeostasis. These findings reveal that KDM6B-H3K27me3-BMI1-PIEZO1 is a critical epigenetic "mechanostat" that protects dental progenitor cells from mechanical stress, ensuring sustained tissue homeostasis. This chromatin-based mechanism of tissue mechano-adaptation could be targeted to prevent mechanically induced degeneration in mineralized tissues. - Source: PubMed
Publication date: 2026/05/28
Meng LinZhang MingyiFeng JifanGuo TingweiHekmat HanaZiaei HeliyaChen PengHarouni AaronHo Thach-VuChai Yang - - Source: PubMed
- Glioblastoma multiforme (GBM) is a lethal and fast-growing brain cancer that is difficult to treat with standard medical interventions. GBM tumors often overexpress cyclin-dependent kinase 9, in complex with cyclin T1, and thus, it represents a promising target for therapeutic intervention. In this study, we employed a structure-based virtual screening approach for a curated library of 6,059 bis-pyridyl compounds from PubChem to identify potential CDK9/T1 inhibitors. Subsequent ADP-Glo assay led to the identification of GNE-3511 as a potent CDK9/T1 inhibitor with an IC of 0.064 μM. GNE-3511 also inhibited CDK7/cyclin H with an IC of 0.12 μM. In U-87 MG and T98G glioblastoma cells, GNE-3511 exhibited cytotoxicity with a GI of 3.4 and 5.0 μM, inducing G2/M phase cell cycle arrest and promoting early apoptosis. Treatment with GNE-3511 significantly reduced the expression of the anti-apoptotic markers BCL-2, SURVIVIN and drug resistance markers ( and ) in a dose-dependent manner, and downregulated glioma stem cell population/markers (, CD90, or CD133 and ) and sphere formation abilities. Oral administration of GNE-3511 at 20 mg/kg (twice daily) demonstrated significant anti-tumor efficacy and improved survival in both U-87 MG and T98G xenograft/orthotopic mouse models. Collectively, these findings highlight GNE-3511 as a promising lead candidate for the development of GBM therapeutics. - Source: PubMed
Publication date: 2026/05/14
Pr Nithya SreeSomarowthu TejaswiS JeyasankariKuncha MadhusudhanaAndugulapati Sai BalajiBharate Sandip B - Natural products and affordable herbal medications have emerged as promising alternatives for cancer therapy, particularly for patients with limited access to standard treatments. Among these, curcumin, the bioactive polyphenol from Curcuma longa (turmeric), has shown broad anti-cancer potential. However, its molecular mechanism remains poorly defined, especially for head and neck squamous cell carcinoma (HNSCC). Here, we identify curcumin as a potent inhibitor of HNSCC tumorigenesis and explored its underlying mechanism. Comparative analyses of three anti-cancer natural products, including curcumin, gingerol, and allicin, revealed that only curcumin robustly inhibited HNSCC cell proliferation, invasion, and cancer stem cell self-renewal, with potency comparable or superior to cisplatin. Transcriptomic and Gene Set Enrichment Analyses demonstrated that curcumin significantly suppressed FOSL1/AP-1 signaling, a well-known key oncogenic signaling that promotes malignant progression of HNSCC. Biophysical and biochemical assays showed that curcumin directly binds to the FOSL1/JUN heterodimer (Kd ≈ 10 μM), disrupting its DNA-binding activity. In agree with this finding, chromatin immunoprecipitation confirmed that curcumin inhibited FOSL1/JUN recruitment to promoter of cancer stem cell marker gene BMI1, as well as super-enhancer-associated oncogenic loci such as MET, EGFR and TP63. At last, curcumin treatment profoundly suppressed HNSCC tumor growth in xenograft model and exhibited superior efficacy compared with the FOSL1/AP-1 inhibitor T-5224, without apparent toxicity. Collectively, our findings identify FOSL1/JUN complex as a direct molecular target of curcumin and uncover a novel mechanism by which this accessible natural product suppresses HNSCC tumorigenesis, supporting its potential as an affordable and safe therapeutic option for cancer treatment. - Source: PubMed
Publication date: 2026/05/07
Li JerryPandit SaritaManupati KanakarajuWang AndrewZaman Shadid UCen Yana - This study evaluated the effects of replacing dietary glucose with fructose on intestinal development in weaned pigs and assessed epithelial growth using a small intestinal organoid model. A total of 26 weaned pigs ([Yorkshire × Landrace] × Duroc, 21 days old) were randomly assigned to three groups: a control group (10 pigs, 3% glucose), a low-fructose (LF) group (8 pigs, 1.5% glucose + 1.5% fructose), and a high-fructose (HF) group (8 pigs, 3% fructose), with one pig per pen. The experimental period lasted 28 d, including a dietary transition on day 15. Results showed that dietary fructose did not affect growth performance (P > 0.10). Fecal scores were not significantly different among treatments (0.05 < P < 0.1), although numerically lower values were observed in the LF group. The HF group had a greater relative length of the large intestine than the LF group (P < 0.05), whereas the LF group showed reduced kidney weight (P < 0.001). Regarding intestinal morphology, dietary fructose tended to reduce duodenal crypt depth and ileal villus height (0.05 < P < 0.1). Ileal malondialdehyde (MDA) levels were affected by dietary treatment (P < 0.05), whereas digestive enzyme activities were not altered (P > 0.10). At the molecular level, fructose significantly downregulated genes involved in carbohydrate metabolism (FBP1, FBP2, LDHA, PKM) and glucose transport (GLUT2) (P < 0.05). Stem cell-associated genes (LGR5 and BMI1) and tight junction-related genes (OCLN and CLDN1) were significantly downregulated (P < 0.05), whereas Ki67 expression was not significantly affected (P > 0.10). In organoid cultures, fructose concentrations did not affect budding efficiency (P > 0.10) but significantly affected the number of buds per organoid (P < 0.05), with higher values observed at 1 mM and 5 mM. Overall, replacing dietary glucose with fructose did not impair growth performance, but altered oxidative status, epithelial-related gene expression, and intestinal epithelial responses in weaned pigs. These findings indicate that intestinal responses are sensitive to dietary monosaccharide composition under practical feeding conditions. - Source: PubMed
Wang MinWang XinZeng YutongGuo MingmingWang ZhaobinYin LanmeiWang QiyeLi JianzhongYang Huansheng