BCL2L11 Antibody
- Known as:
- BCL2L11 Antibody
- Catalog number:
- abx000675
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- BCL2L11 Antibody
Related genes to: BCL2L11 Antibody
- Gene:
- BCL2L11 NIH gene
- Name:
- BCL2 like 11
- Previous symbol:
- -
- Synonyms:
- BOD, BimL, BimEL, BimS, BIM
- Chromosome:
- 2q13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-10
- Date modifiied:
- 2019-04-23
Related products to: BCL2L11 Antibody
Related articles to: BCL2L11 Antibody
- Prostate cancer (PCa) has a high incidence worldwide, yet reliable prognostic biomarkers to distinguish indolent from aggressive forms are lacking. MicroRNAs (miRNAs), a class of small non-coding RNAs, are stable molecules that play an important role in cancer development and can be detected in circulation by non-invasive methods. This study aimed to examine the influence of the cell-free (cf) miRNAs levels on PCa risk and aggressiveness using plasma samples and cell models. Four overexpressed miRNAs in prostate cancer tissue were selected from The Cancer Genome Atlas database: miR-25-3p, miR-92a-1-5p, miR-92a-2-5p, and miR-148a-3p. Cf-miRNA levels were validated via quantitative reverse transcription polymerase chain reaction (RT-qPCR) in plasma samples from 80 PCa patients and 40 controls in a Brazilian cohort. Clinicopathological associations were analyzed to determine prognostic value. Subsequently, functional analyses were performed using transient transfection of miR-25-3p in the LNCaP cell line, assessing proliferation, migration, invasion, and target gene regulation. Among the miRNAs analyzed, only miR-25-3p was upregulated in the plasma of PCa patients compared to controls ( = 0.013). Patients with International Society of Urological Pathology (ISUP) grade ≥2 presented higher expression levels of miR-25-3p ( = 0.020) compared to patients with ISUP grade 1. Overexpression of miR-25-3p significantly increased cell proliferation, colony formation, migration, and invasion capacity and modulated the expression of , , , , and genes. miR-25-3p had an oncogenic role in PCa, showing a potential marker to assess PCa development and progression using liquid biopsy. - Source: PubMed
Publication date: 2026/08/30
Nobrega MonyseKuasne HellenSouza Marilesia Ferreira deReis Mariana Bisarro DosOliveira Larissa Cristina Bastos deFuganti Paulo EmilioPark MoragCólus Ilce Mara de Syllos - Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease with limited medical therapies. The role and targets of icariin, a flavonoid from Epimedium brevicornu Maxim, in AAA remain unclear. First, transcriptomic data from the GEO dataset GSE183464 were analyzed to screen differentially expressed genes (DEGs). DEGs were then integrated with M1 polarizationrelated genes (GeneCards) and icariin-targeted genes (CTD/SwissTargetPrediction) using Venn analysis, and the obtained candidate genes were subjected to GO and KEGG enrichment analyses. Machine learning (LASSO and Random Forest) was employed to prioritize core targets from a gene expression matrix, followed by molecular docking (AutoDock Vina) for assessing the binding affinity between icariin and Cytochrome P450 Family 1 Subfamily B Member 1 (CYP1B1), and visualizing (PyMOL and Discovery Studio) the binding modes. The effects of icariin were evaluated in THP-1-derived macrophages. Bioinformatics identified 15 candidate genes; machine learning converged on CYP1B1/BCL2L11. Molecular docking confirmed icariin's high affinity for CYP1B1. Icariin dose-dependently inhibited LPS/IFN-γ-induced M1 polarization and NF-κB activation, while CYP1B1 overexpression reversed these effects. Icariin also reduced M1-induced VSMC apoptosis. By demonstrating that icariin alleviates AAA by targeting CYP1B1 to suppress NF-κB-driven M1 polarization and VSMC apoptosis, this study establishes the icariin-CYP1B1 axis as a promising therapeutic strategy. - Source: PubMed
Liu XiaosenLi ShuzhenWang JianTian Zexiang - Cisplatin resistance significantly limits chemotherapy options and leads to a poor prognosis in patients with lung adenocarcinoma (LUAD). Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators of drug resistance mechanisms in various tumors. In this study, we investigated the role and underlying molecular mechanism of the focally amplified lncRNA on chromosome 1 (FAL1) in LUAD cisplatin resistance. FAL1 expression levels were measured in blood samples from LUAD patients receiving cisplatin-based chemotherapy and in cisplatin-resistant LUAD cell lines. The functional roles of FAL1 in modulating cisplatin-induced apoptosis and protective autophagy were evaluated using colony formation, flow cytometry, and autophagic flux monitoring assays. Additionally, a xenograft mouse model was employed to assess tumor growth and chemoresistance in vivo. We found that FAL1 levels were significantly elevated in the serum of patients with cisplatin-resistant LUAD and in resistant cell lines. FAL1 knockdown markedly decreased cell proliferation, increased cisplatin-induced apoptosis, and attenuated autophagic flux. Conversely, FAL1 overexpression promoted cell survival and hyperactivated autophagy under cisplatin treatment. Mechanistically, FAL1 stabilized BMI1, leading to the direct transcriptional repression of the pro-apoptotic and autophagy-regulating gene, BCL2-like 11 (BCL2L11/BIM). In vivo experiments confirmed that FAL1 overexpression promoted cisplatin resistance in xenografts via the BMI1/BIM pathway. Taken together, our study demonstrates that FAL1 drives cisplatin resistance in LUAD by shifting the balance between apoptosis and autophagy through the BMI1/BIM axis. These findings highlight FAL1 as a promising therapeutic target to overcome cisplatin resistance in LUAD. - Source: PubMed
Publication date: 2026/07/20
Ma TengXia YangChen YijiangLin HanPan Chunfeng - Carbon nanotubes (CNTs) are carbon-based nanomaterials. They have been widely used in environmental technologies and in biomedical fields. - Source: PubMed
Publication date: 2026/07/01
Lotfipanah ShirinSaremi LeilaRafieitabatabaei YasaminsadatAsgari MasoudHajebrahimi Zahra - House dust mite (HDM) is a major global inducer of allergic asthma, yet its epigenetic impact on airway tissues remains poorly understood. The aim of this study was to perform an exploratory, hypothesis-generating screening of the DNA methylation changes that occur in lung tissue of mice with robust allergic inflammation compared to saline-exposed controls. - Source: PubMed
Publication date: 2026/07/02
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