| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Caspase recruitment domain-containing protein 11; CARD-containing MAGUK protein 3; Carma 1; CARD11; CARMA1 |
| Entrez GeneID | 84433; |
| WB Predicted band size | 130kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse |
| Immunogen | Synthesized peptide derived from internal of human CARD11. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于CARD11抗体的3篇参考文献及其摘要概述：
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1. **文献名称**：*Germline CARD11 Mutation in a Patient with Severe Congenital B Cell Lymphocytosis*
**作者**：Snow, A. L., et al.
**摘要**：该研究报道了一例因CARD11基因功能获得性突变导致的先天性B细胞异常增殖病例。突变引起CARD11蛋白自发激活NF-κB信号通路，导致B细胞过度活化，揭示了CARD11在免疫失调疾病中的关键作用。
2. **文献名称**：*Oncogenic CARD11 Mutations in Human Diffuse Large B Cell Lymphoma*
**作者**：Lenz, G., et al.
**摘要**：通过分析弥漫性大B细胞淋巴瘤(DLBCL)样本，发现CARD11基因的体细胞突变可异常激活NF-κB通路，促进肿瘤细胞存活和增殖，提示CARD11突变是该类癌症的重要驱动因素。
3. **文献名称**：*CARD11-BCL10-MALT1 Signaling in Primary Immunodeficiency Diseases*
**作者**：Turvey, S. E., & Durandy, A.
**摘要**：综述了CARD11信号复合物(CBM)在免疫缺陷中的作用，指出CARD11功能缺失突变会破坏淋巴细胞活化，导致严重联合免疫缺陷(SCID)或反复感染，强调其分子机制及临床表型关联。
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这些文献涵盖了CARD11在肿瘤发生、免疫缺陷及信号通路中的关键作用，适用于基础研究与临床病理机制探讨。如需扩展，可补充针对特定疾病模型或治疗策略的研究。
CARD11 (Caspase Recruitment Domain Family Member 11) is a critical signaling protein in the immune system, primarily expressed in lymphocytes. It plays a central role in antigen receptor-mediated activation of NF-κB, a transcription factor essential for lymphocyte proliferation, survival, and effector functions. Structurally, CARD11 contains a caspase recruitment domain (CARD), a coiled-coil domain, and a MAGUK domain, which facilitate interactions with downstream signaling components like BCL10 and MALT1.
Mutations in the *CARD11* gene are linked to immune dysregulation. Gain-of-function mutations drive constitutive NF-κB activation, associated with B-cell lymphomas and autoimmune disorders. Conversely, loss-of-function mutations cause primary immunodeficiencies, such as severe combined immunodeficiency (SCID) or B-cell expansion defects.
CARD11 antibodies are vital tools in research and diagnostics. They enable detection of CARD11 expression levels, post-translational modifications (e.g., phosphorylation), and abnormal signaling in lymphoid malignancies or immune disorders. In clinical contexts, these antibodies aid in subclassifying lymphomas and identifying patients with CARD11-related mutations, guiding targeted therapies. Therapeutic strategies targeting CARD11 signaling, including inhibitors of the CARD11-BCL10-MALT1 (CBM) complex, are under investigation, highlighting its potential as a drug target. Overall, CARD11 antibodies bridge mechanistic insights into immune signaling with translational applications in oncology and immunology.
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