Ask about this productRelated genes to: BCL2L12 Blocking Peptide
- Gene:
- BCL2L12 NIH gene
- Name:
- BCL2 like 12
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: BCL2L12 Blocking Peptide
Related articles to: BCL2L12 Blocking Peptide
- This study aims to reveal the potential mechanism and potential prognostic markers of programmed cell death (PCD) genes associated with 6-acetoxy-anopterine (6-AA) resistance in prostate adenocarcinoma (PRAD). - Source: PubMed
Publication date: 2026/01/31
Cheng JieMao Dongdong - Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor prognosis and limited treatment options. Synthetic lethality (SL) represents a significant therapeutic strategy that selectively kills cancer cells without affecting normal cells by targeting the synergistic interaction of two genes. The SL strategy offers new avenues for targeted therapy in TNBC. Although challenges remain-such as drug resistance and biomarker selection-advancing research in SL activity holds promise for delivering clinical benefits to patients. - Source: PubMed
Publication date: 2026/02/06
Miao ShichenWang XiaoGu QimingBian ChengyuFan RuiNi QichaoWang YiZhuang Zhigang - Hepatocellular carcinoma (HCC) is a global challenge with a high cancer-related death rate. Although BCL2L12 has been reported to be upregulated in mice with HCC, and its deletion markedly inhibits HCC progression, its specific role and associated tumorigenesis mechanisms in human HCC remain elusive. Differential gene expression analysis was performed using TCGA and GEPIA databases. Survival probability analysis was conducted using the Kaplan-Meier method. Immune checkpoint-related prognosis in HCC and their correlation with BCL2L12 were analyzed. The correlation between BCL2L12 and immune infiltration was investigated using the TIMER database. MEXPRESS and MethSurv were employed to display methylation of BCL2L12 and prognostic value. Upstream ncRNAs of BCL2L12 were predicted using starBase, String and TargetScan. Protein-protein interaction network involving BCL2L12 was constructed via String. Genes related to BCL2L12 in HCC were obtained from the LinkedOmics database. BCL2L12-targeted drugs for HCC were predicted via RNAactDrug, Enrichr, CTD, and NetworkAnalyst. BCL2L12 expression was upregulated and associated with poor prognosis in HCC. BCL2L12 showed significant co-occurrence with an immune checkpoint, namely TNFRSF4. BCL2L12 was significantly associated with immune infiltration in HCC. Cg03848533 methylation and CYTOR/MIR4435-2HG-has-miR-125b-5p axis regulated BCL2L12 expression and prognosis of HCC. BCL2L12 interacted with ZNF215 and PUSL1, all of which were independent risk factors for overall survival in patients with HCC. Panobinostat, Pirinixic acid, and Fluorouracil were predicted to be the potential BCL2L12-targeted drug for HCC. Our findings offer an understanding of the Oncogenic Role of BCL2L12 associated with immune status in the prognosis of HCC and provide potential strategies for currently limited treatment. - Source: PubMed
Publication date: 2025/11/26
Niu KunCao ShuangjiaoLian NanDu RuiLu Guofang - RNA Pol II-mediated transcription is essential for eukaryotic life. Although loss of transcription is thought to be universally lethal, the associated mechanisms promoting cell death are not yet known. Here, we show that death following the loss of RNA Pol II activity does not result from dysregulated gene expression. Instead, it occurs in response to loss of the hypophosphorylated form of Rbp1 (also called RNA Pol IIA). Loss of RNA Pol IIA exclusively activates apoptosis, and expression of a transcriptionally inactive version of Rpb1 rescues cell viability. Using functional genomics, we identify the mechanisms driving lethality following the loss of RNA Pol IIA, which we call the Pol II degradation-dependent apoptotic response (PDAR). Using the genetic dependencies of PDAR, we identify clinically used drugs that owe their lethality to a PDAR-dependent mechanism. Our findings unveil an apoptotic signaling response that contributes to the efficacy of a wide array of anti-cancer therapies. - Source: PubMed
Publication date: 2025/08/15
Harper Nicholas WBirdsall Gavin AHoneywell Megan EWard Kelly MPai Athma ALee Michael J - Efficient cytosolic delivery of nucleic acid therapeutics remains a central challenge for DNA nanostructure-based biomedical applications. Here, we report a programmable DNA origami delivery platformthe DNA Soccer Framework (DSF)cofunctionalized with fluorocarbon chains and sgc8 aptamers to enhance cellular uptake and promote endosomal escape for effective siRNA delivery. Fluorocarbon moieties of tunable lengths and densities were grafted onto DSF to facilitate lipid raft-mediated endocytosis, which favors cytosolic entry by bypassing lysosomal degradation. Concurrently, aptamer comodification enabled selective targeting of cancer cells. Systematic optimization revealed that a surface modification ratio of 3:1 (fluorocarbon to aptamer) among the 90 available sites yielded synergistic improvements in internalization and cytosolic release, significantly enhancing siRNA-mediated gene silencing. Upon loading with siRNA targeting Bcl2L12, the optimized DSF variant induced highest apoptosis in two cancer cell lines, while maintaining minimal cytotoxicity. This work establishes a robust and tunable platform for nucleic acid delivery, advancing the application of DNA nanotechnology in gene therapy and precision medicine. - Source: PubMed
Publication date: 2025/06/22
Zhao LumingLin XiaonaGe NiKuo MinzhanWang ShengwenShi QianBao HongliangYang Yang