纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | Map3k8 |
Uniprot No | P46527 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 30-397aa |
氨基酸序列 | MENLYASEEP AVYEPSLMTM CQDSNQNDER SKSLLLSGQE VPWLSSVRYG TVEDLLAFAN HISNTAKHFY GQRPQESGIL LNMVITPQNG RYQIDSDVLL IPWKLTYRNI GSDFIPRGAF GKVYLAQDIK TKKRMACKLI PVDQFKPSDV EIQACFRHEN IAELYGAVLW GETVHLFMEA GEGGSVLEKL ESCGPMREFE IIWVTKHVLK GLDFLHSKKV IHHDIKPSNI VFMSTKAVLV DFGLSVQMTE DVYFPKDLRG TEIYMSPEVI LCRGHSTKAD IYSLGATLIH MQTGTPPWVK RYPRSAYPSY LYIIHKQAPP LEDIADDCSP GMRELIEASL ERNPNHRPRA ADLLKHEALN |
预测分子量 | 70 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Map3k8(Tpl2/Cot)重组蛋白的3篇参考文献及其摘要概括:
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1. **文献名称**:*Tpl2/Cot信号通路在炎症反应中的调控作用*
**作者**:Dumitru, C. D. 等(1999)
**摘要**:研究揭示了重组Map3k8(Tpl2)蛋白通过激活NF-κB和ERK/MAPK通路调控炎症因子(如TNF-α)的生成,表明其在免疫反应中的关键作用。
2. **文献名称**:*Map3k8重组激酶的体外功能与药物筛选*
**作者**:Cho, J. 等(2005)
**摘要**:通过表达纯化Map3k8重组蛋白,验证其激酶活性及对下游底物MKK1/2的磷酸化能力,为开发靶向Tpl2的抑制剂提供了实验模型。
3. **文献名称**:*Tpl2重组蛋白在白血病细胞增殖中的作用机制*
**作者**:Belicha-Guillermo, N. 等(2011)
**摘要**:利用重组Map3k8蛋白证实其过表达可激活JNK通路并促进白血病细胞增殖,提示其作为癌症治疗潜在靶点的价值。
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以上文献聚焦于Map3k8重组蛋白在信号通路解析、酶活性验证及疾病机制中的功能研究,均为该领域的代表性成果。
The Map3k8 protein, also known as Tpl2 (tumor progression locus 2) or Cot (cancer osaka thyroid), is a serine/threonine kinase belonging to the mitogen-activated protein kinase kinase kinase (MAP3K) family. It plays a critical role in regulating intracellular signaling pathways, particularly the mitogen-activated protein kinase (MAPK) cascades, which mediate cellular responses to cytokines, stress, and growth factors. Map3k8 activates downstream kinases such as MEK1/2 (MAP2K1/2) and subsequently ERK (extracellular signal-regulated kinase), as well as JNK (c-Jun N-terminal kinase) and p38 pathways, influencing processes like inflammation, apoptosis, and cell differentiation. Dysregulation of Map3k8 has been linked to cancer, autoimmune disorders, and inflammatory diseases, making it a therapeutic target of interest.
Recombinant Map3k8 protein is engineered for research applications, typically produced using expression systems like *E. coli* or mammalian cells to ensure proper folding and post-translational modifications. The recombinant form retains the kinase's enzymatic activity, enabling studies on its biochemical properties, substrate interactions, and regulatory mechanisms. Researchers use it to investigate signal transduction pathways, screen kinase inhibitors, or explore its role in immune responses. Structural studies of recombinant Map3k8 have revealed insights into its activation loop, ATP-binding domain, and interaction sites with regulatory proteins like ABIN2 or p105 (NF-κB precursor). Its truncated or mutant variants are also generated to dissect functional domains or mimic disease-associated mutations. As a tool, recombinant Map3k8 aids in deciphering its dual role as both an oncogene and a tumor suppressor, depending on cellular context, while supporting drug discovery efforts aimed at modulating MAPK pathways in inflammatory and neoplastic diseases.
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