BCL2L11 (Human) Recombinant Protein (Q01)
- Known as:
- BCL2L11 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00010018-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BCL2L11 (Human) Recombinant Protein (Q01)
Related genes to: BCL2L11 (Human) Recombinant Protein (Q01)
- 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 (Human) Recombinant Protein (Q01)
Related articles to: BCL2L11 (Human) Recombinant Protein (Q01)
- 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
Llinás-Caballero KevinAcevedo NathalieMerid Simon KebedeDonado KarenEspinoza HectorMondol ErnestoReina RandyRegino RonaldBenedetti InésZakzuk JosefinaPuerta LeonardoMelén ErikCaraballo Luis - Gestational diabetes mellitus (GDM) is a common metabolic disorder of pregnancy associated with placental dysfunction and adverse maternal-fetal outcomes. LncRNAs have emerged as important regulators in metabolic diseases. The clinical significance and molecular mechanisms of lncRNA PANDAR in GDM remain unclear. - Source: PubMed
Publication date: 2026/07/04
Chen LongdingPeng DanpingXu Yunzhi - To investigate the role of BCL-2-interacting mediator of cell death (), a pro-apoptotic molecule, in retinal ganglion cell (RGC) injury after optic nerve crush (ONC), and to analyze its association with changes in the expression of inflammation-related genes. This was an experimental study. The study was conducted from January 2025 to December 2025. Healthy male mice aged 6-8 weeks were randomly divided into four groups: control, ONC, AAV2-scramble, and AAV2-shBim, with 6 mice in each group. The control group received no intervention, the ONC group underwent ONC only, the AAV2-scramble group received intravitreal injection of AAV2-mediated scrambled negative control sequence after ONC, and the AAV2-shBim group received intravitreal injection of AAV2-mediated short hairpin RNA targeting the gene after ONC. Immunohistochemical staining was used to detect the protein expression of Bim, complement component 3 (C3), and lipocalin 2 (Lcn2). Hematoxylin-eosin (HE) staining was used to observe retinal structural changes. Retinal flat-mount immunofluorescence staining was used to assess RGC survival. Optical coherence tomography (OCT) was used to measure ganglion cell complex (GCC) thickness. Flash visual evoked potential (F-VEP) and flash electroretinography (F-ERG) were used to evaluate visual electrophysiological function. RNA sequencing was performed to analyze retinal transcriptomic changes after knockdown. Quantitative real-time PCR (qPCR) was used to validate inflammation-related differentially expressed genes. Independent-sample -test and one-way analysis of variance were used for statistical analysis. The proportions of Bim-positive RGCs in the peripheral and central retina were 0.56±0.06 and 0.63±0.06 in the ONC group, respectively, both of which were higher than those in the control group (0.00±0.00) (=21.60, 24.61; both <0.001). The numbers of RNA-binding protein with multiple splicing(RBPMS)-positive RGCs in the peripheral and central retina were 74.2±4.4 and 118.5±8.0 in the ONC group, respectively, both of which were lower than those in the control group (222.7±6.0 and 325.0±6.5, respectively) (=48.94, 48.88; both <0.001). Significant differences were observed among the four groups in ganglion cell complex thickness, the number of TUJ1-positive RGCs, F-VEP N2-P2 amplitude, and F-ERG b-wave amplitude (=57.42, 1 216.78, 467.88, 423.76; all <0.001). In the AAV2-shBim group, ganglion cell complex thickness, the number of TUJ1-positive RGCs, F-VEP N2-P2 amplitude, and F-ERG b-wave amplitude were 54.64±2.61 μm, 242.8±13.1, 11.13±0.80 μV, and 318.00±25.14 μV, respectively, all of which were higher than those in the ONC group [(44.29±1.95) μm, 140.0±5.3, (3.43±0.48) μV, and (190.68±25.50) μV, respectively] (all <0.001). RNA sequencing showed that the expression levels of the inflammation-related genes , , , , , and were lower in the AAV2-shBim group than in the ONC group (=10.21, 12.02, 8.98, 12.19, 7.33, 9.41; all <0.001), and the quantitative polymerase chain reaction results were consistent with the RNA sequencing results. The C3-positive cell rates in the central and peripheral retina were 0.11±0.04 and 0.08±0.02 in the AAV2-shBim group, respectively, both of which were lower than those in the ONC group (0.64±0.06 and 0.57±0.05, respectively) (=18.63, 21.04; both <0.001). The Lcn2-positive cell rates in the central and peripheral retina were 0.08±0.03 and 0.09±0.02 in the AAV2-shBim group, respectively, both of which were lower than those in the ONC group (0.55±0.06 and 0.48±0.07, respectively) (=17.19, 12.38; both <0.001). expression is upregulated after ONC. AAV2-mediated knockdown alleviates RGC loss, retinal structural damage, and visual electrophysiological dysfunction, accompanied by downregulation of inflammation-related gene expression. - Source: PubMed
Cheng Z HChen X NLi Z H