c_FLIP pAb;human, mouse, rat
- Known as:
- c_FLIP pAb;H. sapiens, mouse, rat
- Catalog number:
- ASAAAP-440E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- c_FLIP pAb;human mouse rat
Related genes to: c_FLIP pAb;human, mouse, rat
- Gene:
- CFLAR NIH gene
- Name:
- CASP8 and FADD like apoptosis regulator
- Previous symbol:
- CASP8AP1
- Synonyms:
- CASH, Casper, CLARP, FLAME, FLIP, I-FLICE, MRIT, c-FLIP, cFLIP
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2019-02-25
Related products to: c_FLIP pAb;human, mouse, rat
Related articles to: c_FLIP pAb;human, mouse, rat
- Diffuse large B cell lymphoma (DLBCL) is a highly heterogenous malignant disease that remains a major clinical challenge as relapsed and refractory disease is difficult to treat. Apoptosis evasion is a major feature of DLBCL. However, while the suppression of intrinsic apoptosis has long been recognized as a lymphoma-promoting event, the role of extrinsic apoptosis has remained poorly defined. Here, we demonstrated at the genetic level that expression of cFLIP, the most crucial, non-redundant inhibitor of extrinsic apoptosis, in B cells is necessary for the development of diffuse large B cell lymphoma (DLBCL) in an autochthonous murine model. Indeed, B cell-specific deletion of Cflar, the gene encoding for cFLIP, prevented lymphomagenesis mediated by oncogenic Myd88 and overexpression of BCL2. In human lymphoma cells, we showed that the absence of cFLIP sensitizes ABC- but not GCB DLBCL subtype cells to TRAIL- or LPS-induced, Caspase-8-mediated apoptosis. Furthermore, we unveiled a cell death-independent role of cFLIP in the suppression of pro-inflammatory cytokines at the transcriptional level, selectively in the ABC subtype.These results indicate that the suppression of intrinsic apoptosis can support lymphomagenesis only if extrinsic apoptosis is properly controlled. Moreover, licensing extrinsic apoptosis via cFLIP deletion can efficiently promote the death of DLBCL cells despite the suppression of the intrinsic pathway. Overall, these data provide the rationale for the development of cFLIP inhibitors for the treatment of ABC DLBCL and possibly other haematological cancers. - Source: PubMed
Publication date: 2026/04/23
Bariboloka Kristie TanavuraSerrano-Saenz SantiagoSavcigil Deniz PinarSpoeck SarahPoss Rebecca ESchreurs Luca DLöber JensSerin NazliValiulis JustinasNugraha KalvinGangarossa GiuliaLütz AnnaReese MoritzKlein SebastianEnssle Julius CBüttner ReinhardKashkar HamidPeifer MartinChapuy BjörnKnittel GeroLabi VerenaVillunger AndreasNguyen Phuong-HienScheich SebastianOellerich ThomasWalczak HenningFlümann RuthJachimowicz Ron DHallek Michael JReinhardt Hans ChristianAnnibaldi Alessandro - Chronic Lymphocytic Leukemia (CLL) is a genetically complex and clinically heterogeneous hematologic malignancy characterized by clonal proliferation of mature B-cells. Though a number of genome-wide association analyses (GWAS) have identified several susceptibility loci associated with CLL, much of its inherited risk remains unexplored. In this study, we combined summary statistics of multiple GWAS to identify some novel genetic risk factors associated with CLL. Firstly, we identified 2357 significant single nucleotide polymorphisms (SNPs) associated with CLL by using the threshold at -value < 5 × 10 computed with the METAL web-tool. Then we functionally mapped and annotated these significant SNPs using Linkage Disequilibrium (LD)-based annotation in FUMA, and obtained 204 independent, 59 lead, and 2,075 candidate SNPs across 40 genomic risk loci. The positional and eQTL mapping were performed with candidate SNPs, and we found 60 unique genes. Subsequently, we identified 7 genes (TERT, BCL2L11, FAS, BCL2, CFLAR, CASP8, and LEF1) as the CLL-associated key genes (KGs) by the protein-protein interaction (PPI) network analysis. The KGs-CLL relationship was also supported by DisGNET. KGs-regulatory network analysis identified some key transcription factors and microRNAs as the transcriptional and post-transcriptional regulators. KGs-set enrichment analysis using gene ontology (GO) and KEGG pathways revealed some key biological processes, molecular functions, cellular components, and signaling pathways. All KGs were found to be druggable and showed known drug-gene interactions. Finally, four candidate drug agents guided by KGs, were proposed for CLL. Hence, the results of this study could become valuable assets for the diagnosis and therapies of patients with CLL. - Source: PubMed
Publication date: 2026/03/23
Islam Md SharifulMollah Md Manir HossainAhsan Md AsifAli MohammadAl Noman MdAhmed Md FoysalLatif Md AbdulPal Nibas KumarFaysal Md FahimMollah Md Nurul Haque - Prostate cancer is a leading cause of cancer-associated death in men worldwide. Inhibition of the Cellular FLICE-like Inhibitory Protein (cFLIP), which is overexpressed in prostate cancer, alongside TRAIL treatment can trigger apoptosis and suppress cancer stem cell (CSC) activity in different cancer types but has not been fully explored in prostate cancer. - Source: PubMed
Publication date: 2026/03/03
Turnham Daniel JFrench RhiannonFrame Fiona MMeniel Valerie SMaitland Norman JClarkson Richard W E - Colorectal cancer (CRC) is a malignant disease that poses a significant threat to human health; however, early diagnostic and treatment strategies for it remain limited. Immune evasion is a critical factor contributing to treatment failure in CRC. Various cell subtypes within the tumor microenvironment (TME) play essential roles in this process. However, there is currently a lack of a systematic and novel classification of immune evasion-related cell subtypes and an analysis of their dynamic interaction networks within the CRC TME. This study aims to explore a novel classification of immune evasion-related subtypes in CRC, elucidate their underlying mechanisms, and assess their value for immunotherapy and prognosis. - Source: PubMed
Publication date: 2026/01/21
Gan QixinXu XuanLiu HaifenLi Yuejun - Ischemic stroke is a cerebrovascular disease that can cause long-term neurological impairment, dementia, or death. It is the third most common cause of disability and the second leading cause of death worldwide. The aim of this study was to explore the underlying molecular mechanisms and potentially effective therapeutic drugs for ischemic stroke. Single-cell seq data (GSE174574) were downloaded from the Gene Expression Omnibus (GEO) database, and dimensionality reduction clustering was performed after quality control. Eighteen cell clusters were identified, which were annotated into 9 cell types according to specific marker genes. In addition, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) enrichment analysis showed that apoptosis was significantly increased after ischemic brain injury, while p53 signaling pathway, TNF-a signaling pathway and mitogen-activated protein kinase (MAPK) signaling pathway may play an important role in ischemic stroke. Furthermore, Connectivity Map (CMap) analysis and molecular docking suggested that piperlongumine might be an effective drug for the treatment of ischemic stroke by binding to the proteins encoded by Actb and Cflar. Finally, in vitro and in vivo experiments conformed the effectiveness of piperlongumine. This study provided new ideas for the treatment of ischemic stroke. - Source: PubMed
Publication date: 2026/01/23
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