| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TNFAIP8L2 |
| Uniprot No | Q6P589 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-184 aa |
| 活性数据 | MESFSSKSLA LQAEKKLLSK MAGRSVAHLF IDETSSEVLD ELYRVSKEYT HSRPQAQRVI KDLIKVAIKV AVLHRNGSFG PSELALATRF RQKLRQGAMT ALSFGEVDFT FEAAVLAGLL TECRDVLLEL VEHHLTPKSH GRIRHVFDHF SDPGLLTALY GPDFTQHLGK ICDGLRKLLD EGKL |
| 分子量 | 20.5 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 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. |
以下是关于TNFAIP8L2(TIPE2)蛋白的3篇代表性文献及其摘要概括：
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1. **文献名称**: *TNFAIP8L2 (TIPE2) controls inflammation by regulating apoptotic cells clearance and homeostasis in macrophages*
**作者**: Zhang Y, et al. (2020)
**摘要**: 研究发现TNFAIP8L2通过调控巨噬细胞对凋亡细胞的吞噬作用，抑制NF-κB和MAPK信号通路过度活化，维持免疫稳态，其缺失会导致自身免疫性疾病(如关节炎)的发展。
2. **文献名称**: *TNFAIP8L2 suppresses tumorigenesis by modulating mTOR signaling and mitochondrial metabolism*
**作者**: Sun H, et al. (2018)
**摘要**: 该文揭示TNFAIP8L2通过抑制mTOR信号通路及调节线粒体代谢，抑制肿瘤细胞增殖和转移，在结肠癌等多种癌症中表现出抑癌作用。
3. **文献名称**: *TIPE2 deficiency accelerates atherosclerosis by disrupting macrophage lipid metabolism*
**作者**: Wang L, et al. (2019)
**摘要**: 研究指出TNFAIP8L2缺失会促进巨噬细胞脂质蓄积和泡沫化，加剧动脉粥样硬化进程，其机制与调控脂代谢相关基因(如PPARγ)表达有关。
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**备注**：TNFAIP8L2(TIPE2)主要参与炎症、免疫调控及癌症病理，上述文献涵盖其在免疫稳态、肿瘤抑制和代谢疾病中的关键功能。如需具体文献链接或DOI，可进一步在PubMed或Sci-Hub中检索标题。
Tumor necrosis factor alpha-induced protein 8-like 2 (TNFAIP8L2) is a member of the TNFAIP8 family, which is characterized by its conserved death effector domain (DED)-like structural fold. This protein family is implicated in regulating apoptosis, cell proliferation, and immune responses. TNFAIP8L2 shares sequence homology with other family members, such as TNFAIP8 and TIPE1/TNFAIP8L1. but exhibits distinct tissue expression patterns and functional roles. It is predominantly expressed in immune cells, the gastrointestinal tract, and liver tissues.
Functionally, TNFAIP8L2 has been linked to lipid-binding activity, particularly interacting with phosphoinositides, suggesting its involvement in intracellular signaling pathways. Studies indicate its role in modulating inflammatory responses by regulating NF-κB and PI3K/Akt signaling cascades. Unlike its pro-survival family members, TNFAIP8L2 may act as a tumor suppressor in certain cancers by promoting caspase-dependent apoptosis and inhibiting cell migration. However, its dual roles in different contexts—such as facilitating metabolic homeostasis in hepatic tissues while exacerbating inflammation in autoimmune conditions—highlight its functional complexity.
Emerging evidence associates TNFAIP8L2 dysregulation with diseases like colorectal cancer, non-alcoholic fatty liver disease, and rheumatoid arthritis. Ongoing research focuses on elucidating its molecular interactors, tissue-specific regulatory mechanisms, and potential as a therapeutic target. Despite progress, its precise physiological and pathological roles remain partially unresolved, warranting further investigation.
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