癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
MEK4 (MAP2K4) Antibody (S257)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | P45985 |
| Other Accession | P47809, Q07192 |
| Reactivity | Human |
| Predicted | Mouse, Xenopus |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 44288 Da |
| Antigen Region | 235-264 aa |
| Gene ID | 6416 |
|---|---|
| Other Names | Dual specificity mitogen-activated protein kinase kinase 4, MAP kinase kinase 4, MAPKK 4, JNK-activating kinase 1, MAPK/ERK kinase 4, MEK 4, SAPK/ERK kinase 1, SEK1, Stress-activated protein kinase kinase 1, SAPK kinase 1, SAPKK-1, SAPKK1, c-Jun N-terminal kinase kinase 1, JNKK, MAP2K4, JNKK1, MEK4, MKK4, PRKMK4, SEK1, SERK1, SKK1 |
| Target/Specificity | This MEK4(MAP2K4) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 235-264 amino acids from human MEK4(MAP2K4). |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | MEK4 (MAP2K4) Antibody (S257) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | MAP2K4 |
|---|---|
| Synonyms | JNKK1, MEK4, MKK4, PRKMK4, SEK1, SERK1, |
| Function | Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. With MAP2K7/MKK7, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3. MAP2K4/MKK4 and MAP2K7/MKK7 both activate the JNKs by phosphorylation, but they differ in their preference for the phosphorylation site in the Thr-Pro-Tyr motif. MAP2K4 shows preference for phosphorylation of the Tyr residue and MAP2K7/MKK7 for the Thr residue. The phosphorylation of the Thr residue by MAP2K7/MKK7 seems to be the prerequisite for JNK activation at least in response to pro-inflammatory cytokines, while other stimuli activate both MAP2K4/MKK4 and MAP2K7/MKK7 which synergistically phosphorylate JNKs. MAP2K4 is required for maintaining peripheral lymphoid homeostasis. The MKK/JNK signaling pathway is also involved in mitochondrial death signaling pathway, including the release cytochrome c, leading to apoptosis. Whereas MAP2K7/MKK7 exclusively activates JNKs, MAP2K4/MKK4 additionally activates the p38 MAPKs MAPK11, MAPK12, MAPK13 and MAPK14. |
| Cellular Location | Cytoplasm. Nucleus. |
| Tissue Location | Abundant expression is seen in the skeletal muscle. It is also widely expressed in other tissues |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
MAP2K4 is a dual specificity protein kinase that belongs to the Ser/Thr protein kinase family. This kinase is a direct activator of MAP kinases in response to various environmental stresses or mitogenic stimuli. It has been shown to activate MAPK8/JNK1, MAPK9/JNK2, and MAPK14/p38, but not MAPK1/ERK2 or MAPK3/ERK3. MAP2K4 is phosphorylated, and thus activated by MAP3K1/MEKK. The knockout studies in mice suggested the roles of this kinase in mediating survival signal in T cell development, as well as in the organogenesis of liver.
REFERENCES
Robinson,V.L.,Mol. Cancer Res. 6 (3), 501-508 (2008)
Zhang,H.,J. Biol. Chem. 282 (20), 14788-14796 (2007)
Salmeron,A.,EMBO J. 15 (4), 817-826 (1996)
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