BCL2L11 Antibody (Center)
- Known as:
- BCL2L11 Antibody (Center)
- Catalog number:
- AP8553c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- BCL2L11 Antibody (Center)
Related genes to: BCL2L11 Antibody (Center)
- 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 (Center)
Related articles to: BCL2L11 Antibody (Center)
- 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 - Osteonecrosis and fractures are serious corticosteroid-induced bone toxicities in children treated for acute lymphoblastic leukemia, yet their genetic determinants remain incompletely defined. In this study, we aimed to identify novel genetic contributors to bone toxicity and to evaluate the robustness of both newly identified and previously established risk genotypes in more recent Dana-Farber Cancer Institute treatment protocols. Whole-exome sequencing was first performed in a discovery cohort to identify genetic variants associated with osteonecrosis. A novel association with a variant in the PGAP2 gene was identified and subsequently confirmed in an independent replication cohort, with effects of patient- and disease-related characteristics observed in both cohorts. Next, previously reported candidate gene-derived associations, together with this newly identified variant, were assessed in a more recent cohort to examine their relevance in contemporary treatment protocols. Variants in BCL2L11 and the ACP1-SH3YL1 locus were associated with bone fractures, with a strong synergistic effect and significant modulation by protocol-specific factors, particularly corticosteroid exposure and asparaginase formulation. The PGAP2 variant was associated with the combined osteonecrosis-fracture phenotype. Transcriptomic analyses revealed isoform-specific expression shifts in PGAP2 in patients with osteotoxicity, supporting a potential functional role for altered splicing or gene regulation. Together, our results provide insight into the pharmacogenomic architecture of osteotoxicity in ALL, demonstrating that PGAP2, BCL2L11, and ACP1-SH3YL1 variants remain clinically relevant predictors of bone toxicity across evolving treatment protocols. However, their clinical manifestations appear to be context-dependent, underscoring the importance of integrating genetic susceptibility with pharmacologic exposures and supporting further investigation of the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/06/22
Abaji RachidGagné VincentEspagne ÉmilieAlos NathalieDel Vecchio VeronicaAit Said LamiaShalmiev AlbertFuchs ClaireLaverdière CarolineLeclerc Jean-MarieSallan Stephen ESilverman Lewis BSinnett DanielTran Thai HoaKrajinovic Maja - miRNA is a small intranuclear noncoding RNA, approximately 22 nucleotides (nt), that is aberrantly expressed in tumor cells and tissues. They play important regulatory roles in cell proliferation and chemosensitivity. Our study focuses on the expression of miR-4295 and its role in gastric cancer. - Source: PubMed
Publication date: 2026/06/10
Yang XiaoyanWei LiushanFeng YuhuiLei XiaoYong - Glioblastoma is an aggressive primary brain tumor characterized by high recurrence rates and resistance to standard therapies, including temozolomide (TMZ). Emerging evidence suggests that microRNAs (miRNAs) play a critical role in regulating treatment response and tumor progression. In this study, we investigated the effects of TMZ and the JAK inhibitor ruxolitinib, alone and in combination, on miRNA expression profiles in glioblastoma cancer stem cells. miRNA expression levels were analyzed using quantitative real-time PCR, and differential expression was evaluated using the 2 method. TMZ treatment increased the expression of oncogenic miRNAs, including hsa-miR-19a-3p, hsa-miR-221-3p, and hsa-miR-10a-5p, whereas ruxolitinib treatment reduced their expression levels. Combination treatment attenuated the TMZ-induced upregulation of these miRNAs. Bioinformatics analyses were performed to identify target genes and associated signaling pathways. Predicted targets were obtained using TargetScan and further supported by experimentally validated interactions from miRTarBase. KEGG pathway enrichment analysis revealed significant associations with cancer-related pathways, including PI3K-Akt, MAPK, Wnt, and Hippo signaling pathways. Network analysis highlighted key genes such as BCL2L11, PTEN, and SOCS family members. Overall, our findings suggest that TMZ may induce oncogenic miRNA expression as part of an adaptive response, while ruxolitinib may counteract this effect. Targeting miRNA-mediated regulatory networks in combination with pathway inhibition may represent a promising strategy to overcome therapeutic resistance in glioblastoma. - Source: PubMed
Publication date: 2026/06/08
Ozates Neslihan PinarAsik AycanBagca Bakiye GokerAvci Cigir Biray - Acute lymphoblastic leukemia (ALL) is a clinically diverse cancer in which microRNA (miRNA)-mediated post-transcriptional regulation contributes to leukemogenesis and subtype heterogeneity. In this study, miRNA expression profiling by microarray was performed on ALL cases (B-ALL and T-ALL) and healthy controls. Data were normalized and analyzed for differential expression using false discovery rate (FDR)-adjusted -values. Differentially expressed miRNAs were further examined using unsupervised visualization to assess overall disease-related expression patterns. To explore their biological significance, experimentally validated miRNA-target interactions were obtained using multiMiR, limited to validated databases (miRTarBase, TarBase, and miRecords) and summarized via target-burden ranking, miRNA-target network analysis, and Circos-style interaction mapping. A unique miRNA expression signature was identified in ALL. Upregulated miRNAs included miR-106a-5p, miR-106b-5p, miR-17-5p, miR-20a-5p, miR-20b-5p, miR-181b-5p, and miR-128-3p, while miR-127-3p, miR-139-5p, miR-433-3p, and miR-584-5p were downregulated. Validated targets concentrated on key leukemia-related genes like PTEN, BCL2L11, CDKN1A, CCND1, RB1, E2F1, and TGFBR2. KEGG pathway analysis highlighted pathways associated with leukemic cell survival and growth, including MAPK, cell cycle, autophagy, Hippo, ubiquitin-mediated proteolysis, and mTOR signaling pathways. These findings reveal a concise ALL-associated miRNA panel predominantly comprising the miR-17/20/106 family and provide a prioritized set of candidate regulatory networks for subtype-specific validation and functional follow-up studies. - Source: PubMed
Publication date: 2026/04/27
Basingab Fatemah SAlahdal HadilAlwadaani DeemahAlmuneef GhaidaBarefah Ahmed SAlgiraigri Ali HHammad RawanElnakeeb MohamedAlrahimi Jehan SZaher Kawther AAldahlawi Alia M