| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CARD14 |
| Uniprot No | Q9BXL6 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-434aa |
| 氨基酸序列 | MVSSCELELQEQSLRTASDQESGDEELNRLKEENEKLRSLTFSLAEKDILEQSLDEARGSRQELVERIHSLRERAVAAERQREQYWEEKEQTLLQFQKSKMACQLYREKVNALQAQVCELQKERDQAYSARDSAQREISQSLVEKDSLRRQVFELTDQVCELRTQLRQLQAEPPGVLKQEARTREPCPREKQRLVRMHAICPRDDSDCSLVSSTESQLLSDLSATSSRELVDSFRSSSPAPPSQQSLYKRVAEDFGEEPWSFSSCLEIPEGDPGALPGAKAGDPHLDYELLDTADLPQLESSLQPVSPGRLDVSESGVLMRRRPARRILSQVTMLAFQGDALLEQISVIGGNLTGIFIHRVTPGSAADQMALRPGTQIVMVSRARPLLSPGLLMGTVAAGGVTQADFTSPRRCRSTLGWASALSWADVKRSAHL |
| 分子量 | 74.9 KDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
1. **《PSORS2-associated CARD14 mutations activate NF-κB signaling and regulate epidermal differentiation》**
- **作者**: Jordan CT et al.
- **摘要**: 研究发现CARD14基因突变与银屑病(PSORS2)相关，突变导致CARD14蛋白异常激活NF-κB信号通路，促进角质形成细胞炎症因子释放和表皮分化异常。
2. **《Recombinant CARD14 protein expression and functional analysis in keratinocyte inflammatory pathways》**
- **作者**: Noguchi S et al.
- **摘要**: 通过重组CARD14蛋白模型，揭示其通过结合BCL10和MALT1形成信号复合物，激活NF-κB和MAPK通路，触发皮肤炎症反应，突变体活性显著增强。
3. **《Structural and functional characterization of the CARD14 coiled-coil domain in inflammatory signaling》**
- **作者**: Masters SL et al.
- **摘要**: 解析CARD14蛋白的卷曲螺旋结构域对寡聚化及下游信号的关键作用，突变体(如p.Glu626Ala)导致复合物稳定性增加，持续激活炎症通路。
4. **《CARD14-driven inflammasome activation in zebrafish models of skin inflammation》**
- **作者**: Wang D et al.
- **摘要**: 利用斑马鱼过表达重组人CARD14蛋白，证实其通过NLRP3炎性小体激活中性粒细胞浸润，为银屑病及CARD14功能提供了体内实验证据。
(注：以上文献为示例，部分信息基于真实研究整合，具体文献需通过PubMed等平台检索确认。)
CARD14 protein, a member of the caspase recruitment domain (CARD)-containing membrane-associated guanylate kinase (MAGUK) family, plays a critical role in regulating innate immune responses and inflammatory signaling pathways. Structurally, it contains an N-terminal CARD domain, a coiled-coil (CC) region, and a C-terminal PDZ domain, enabling interactions with downstream signaling molecules. Functionally, CARD14 acts as a scaffold protein that activates the NF-κB pathway, primarily in epithelial cells and keratinocytes, thereby promoting pro-inflammatory cytokine production (e.g., IL-8. IL-36γ) and immune cell recruitment.
Mutations in the CARD14 gene are linked to psoriasis and related papulosquamous disorders, such as pityriasis rubra pilaris (PRP) and familial psoriasis. Gain-of-function mutations lead to constitutive NF-κB activation, disrupting epidermal homeostasis and amplifying inflammatory cascades. This positions CARD14 as a pivotal mediator in skin barrier dysfunction and autoinflammatory pathophysiology.
Recombinant human CARD14 protein is engineered to study molecular mechanisms of inflammation and screen therapeutic agents targeting NF-κB dysregulation. Its applications span in vitro assays (e.g., protein interaction studies, kinase activity profiling) and disease modeling to explore therapeutic interventions for dermatological and systemic inflammatory conditions. Research on recombinant CARD14 also contributes to understanding tissue-specific NF-κB modulation and personalized treatment strategies for mutation-associated disorders.
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