BMI1 Antibody
- Known as:
- BMI1 Antibody
- Catalog number:
- 32015
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- BMI1 Antibody
Related genes to: BMI1 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 Antibody
Related articles to: BMI1 Antibody
- 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 days, 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
Publication date: 2026/05/07
Wang MinWang XinZeng YutongGuo MingmingWang ZhaobinYin LanmeiWang QiyeLi JianzhongYang Huansheng - The high incidence and recurrence of hepatoma necessitate better prognostic tools. Given the established cytotoxic role of CD4+ T cells, this study aimed to identify CD4+ T cell-related genes (TRGs) and their mechanisms in hepatoma. - Source: PubMed
Publication date: 2026/04/27
Zhang ZheweiGuo LiwenLuo JunZheng JiapingZeng Hui - Radiation-induced intestinal injury is a widely used model for studying mechanisms regulating tissue injury and regeneration. Traditionally, Cesium ( Cs) radiation has been used in research applications, but over the past decade, X-ray irradiation has become increasingly favored due to its improved safety and non-radioactive profile. Since each type of radiation has distinct physical characteristics that drive its performance, we sought to systematically compare the effects of the X-ray and Cs irradiators on intestinal epithelial injury and regeneration. Using established models, including colorectal cancer cell lines such as HCT116, RKO, and DLD-1, and mouse intestinal organoids, alongside model, ; , we evaluated differences in transcriptional, protein, and histopathological responses to irradiation. Our results demonstrate that X-ray produced intestinal injury and regenerative responses comparable to those induced by Cs, supporting its reliability as an alternative modality for studying intestinal radiation. - Source: PubMed
Publication date: 2026/04/21
Lakha RabinaOrzechowska-Licari Emilia JKesavan SahaanaWu Zhi JRotoli MatthewGiarrizzo MichaelYang Vincent WBialkowska Agnieszka B