CARD11 antibody
- Known as:
- CARD11 (anti-)
- Catalog number:
- orb100334
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CARD11 antibody
Related genes to: CARD11 antibody
- Gene:
- CARD11 NIH gene
- Name:
- caspase recruitment domain family member 11
- Previous symbol:
- -
- Synonyms:
- CARMA1, BIMP3
- Chromosome:
- 7p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-13
- Date modifiied:
- 2019-04-23
Related products to: CARD11 antibody
Related articles to: CARD11 antibody
- Diffuse large B-cell lymphoma (DLBCL) can be subclassified by phenotype into germinal center B-cell-like and activated B-cell-like (ABC) subtypes and by recurrent potentially oncogenic mutations into 5 to 7 genetic clusters. In ABC-DLBCL, potentially oncogenic mutations frequently occur in genes involved in B-cell receptor (BCR) signaling and NF-κB activation. Autonomous BCR signaling acts as an alternative immunologic driver predominantly in ABC-type DLBCL that cannot be captured by either subclassification system. The relative functional contribution and interdependence of these mechanistically diverse oncogenic drivers have not been completely defined. To directly compare the effects of autonomously signaling BCR and signalosome-activating CARD11 mutations on NF-κB activation and survival of ABC-DLBCL, we reciprocally exchanged these driver mechanisms in the MYD88-mutated ABC-DLBCL cell lines TMD8 and OCI-Ly3. Only CARD11 (not CARD11, CARD11, and CARD11) compensated TMD8 cells for the loss of autonomous BCR signaling, as indicated by survival of BCR knockout and conversion to complete resistance to acalabrutinib. Transduction of the TMD8 BCR rescued OCI-Ly3 cells from replacing the CARD11 variant with CARD11. The autonomous TMD8 BCR signal provided a slight growth advantage over CARD11-driven cells in both reciprocal systems. Unsupervised clustering of genetically engineered TMD8 and OCI-Ly3 clones demonstrated tight clustering with their parental cells and only minor alterations of cellular pathways. Only the strongest signalosome-activating mutation has functional near-equivalency to an autonomously signaling BCR for NF-κB activation and growth and survival in ABC-DLBCL. Quantifying the effects of co-occurring potential NF-κB-activating mechanisms is essential to predict Bruton tyrosine kinase (BTK) inhibition sensitivity in individual ABC-DLBCL cases. - Source: PubMed
Publication date: 2026/06/25
Eken Janneke AHavenaar Fleur R Mde Groen Ruben A LQuinten EdwinMei HailiangSepúlveda-Yáñez Julieta HNavarrete Marcelo ADrexler Hans GVermaat Joost S Pvan Bergen Cornelis A MVeelken Hendrik - To investigate the gene mutations in tumor tissues of patients with primary gastrointestinal diffuse large B-cell lymphoma (PGI-DLBCL), and analyze its relationship with clinical features and prognosis. - Source: PubMed
Kou ZhenLin Si-YingQi Xiao-LongRe NaguliTan WeiWang Zeng-ShengGu Zailinuer - Adult T cell leukemia/lymphoma (ATL) is an aggressive T cell malignancy with poor prognosis. Recurrent genetic alterations in T cell receptor (TCR) signaling components, including , , and , highlight the biological relevance of this pathway in ATL. We focused on mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), a key regulator of TCR signaling that functions through complex formation with CARD11 and BCL10, and developed a potent and selective MALT1 protease inhibitor, CRD-1441551. CRD-1441551 exhibited variable antitumor effects across ATL models both and . Among three ATL cell lines and five patient-derived xenograft models, two demonstrated marked sensitivity, three showed modest responses, and three were unresponsive. Notably, therapeutic responses were more frequently observed in models with constitutive MALT1 activation accompanied by enhanced MALT1-NF-κB signaling. These findings suggest that CRD-1441551 preferentially targets a subset of ATL, in which tumor growth is dependent on the MALT1-driven NF-κB pathway. - Source: PubMed
Publication date: 2026/07/23
Kamiunten AyakoMorishita DaisukeKameda TakuroSugiyama MidoriEbara ShunsukeKogure YasunoriMizutani AkioHirayama TakaharuKawamoto TomohiroOchi YotaroShide KotaroTokuhara HidekazuTanaka ToshioBanno HiroshiArikawa YasuyoshiMaru TakamitsuOki HideyukiYoda AkinoriTahira YukiIkeda RyomaMatsumoto KengoKarasawa MasayoshiAkizuki KeiichiSekine MasaakiShimoda HarukoHidaka TomonoriKubuki YokoYamaguchi HidekiHasegawa HirooImaizumi YoshitakaYasunaga Jun-IchirouMatsuoka MasaoYoshimitsu MakotoIshitsuka KenjiKataoka KeisukeOgawa SeishiShimoda Kazuya - Autism spectrum disorder (ASD) is a genetically complex neurodevelopmental condition with a high heritability. However, genomic studies of ASD have been underrepresented in East Asian populations, and the molecular yield in ASD cohorts remains modest. Here, we present a whole-genome sequencing analysis of 3109 samples across 1033 Chinese ASD families. By examining a wide spectrum of genetic variation, we identified rare ASD-associated variants in 19.2% of affected individuals, providing a population-specific view of the genetic architecture of ASD. We identify significant enrichment of de novo variants in probands, nominate or strengthen candidate risk genes (e.g., NCL, SPPL3, ADGRB1, SLC9A3, KIF1B) through mutational burden, evolutionary constraint, recurrent missense site, and functional assays, and implicate convergent pathways including protein palmitoylation. By integrating over 40,000 ASD cases across unpublished and published global cohorts, we identify 245 ASD risk genes, including 45 with limited prior evidence and 32 with no prior association. Single-cell transcriptomic profiling of the developing human cortex reveals that ASD risk genes exhibit widespread yet heterogeneous expression across all major cell types, with peak expression in excitatory neurons, particularly intratelencephalic neurons, and enriched expression in microglia (e.g., C1QC, CARD11, SNX13, MEF2C, FOXP2, TCF12, MED13L), suggesting convergent involvement of both synaptic and neuroimmune mechanisms. Together, our findings expand the ASD genetic landscape and suggest convergent pathogenic axes involving transcriptional regulation, synaptic signaling and plasticity, and neuroimmune interactions. This work supports the development of inclusive diagnostic strategies and provides a foundation for mechanistic and intervention exploration in ASD. - Source: PubMed
Publication date: 2026/07/16
Tan SenweiLyu YongqingSun XiaoyueGuo RuolanZhang XiaoleiSong ZhuoChen KewenLi ChenzhangZheng YiJiang CanhuiQin CaiBai TingTang GuizhiLi JuanLong ZhigaoPan QianTan JieqiongZhao NingxiaHao YanZhang YuShen YidongOu JianjunCui YonghuaHao ChanjuanJia XiangbinXia LuLi JinchenHu ZhengmaoLi WeiGuo HuiXia Kun - - Source: PubMed
Publication date: 2026/07/15
Zangari PaolaManno Emma ConcettaDe Luca MaiaMancinelli LiviaOnori ManuelaLepanto Maria StefaniaBernaschi PaolaRotulo Gioacchino Andrea