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。
COT (MAP3K8/MEKK8) Antibody (C-term) 精选
Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | P41279 |
| Reactivity | Human |
| Predicted | Mouse, Rat, Bovine, Canine, Rabbit |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 52925 Da |
| Antigen Region | 414-445 aa |
| Gene ID | 1326 |
|---|---|
| Other Names | Mitogen-activated protein kinase kinase kinase 8, Cancer Osaka thyroid oncogene, Proto-oncogene c-Cot, Serine/threonine-protein kinase cot, Tumor progression locus 2, TPL-2, MAP3K8, COT, ESTF |
| Target/Specificity | This COT (MAP3K8/MEKK8) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 414-445 amino acids from the C-terminal region of human COT (MAP3K8/MEKK8). |
| 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 prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| 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 | COT (MAP3K8/MEKK8) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | MAP3K8 |
|---|---|
| Synonyms | COT, ESTF |
| Function | Required for lipopolysaccharide (LPS)-induced, TLR4-mediated activation of the MAPK/ERK pathway in macrophages, thus being critical for production of the pro-inflammatory cytokine TNF (TNF) during immune responses. Involved in the regulation of T-helper cell differentiation and IFNG expression in T-cells. Involved in mediating host resistance to bacterial infection through negative regulation of type I interferon (IFN) production. In vitro, activates MAPK/ERK pathway in response to IL1 in an IRAK1-independent manner, leading to up-regulation of IL8 and CCL4. Transduces CD40 and TNFRSF1A signals that activate ERK in B-cells and macrophages, and thus may play a role in the regulation of immunoglobulin production. May also play a role in the transduction of TNF signals that activate JNK and NF-kappa-B in some cell types. In adipocytes, activates MAPK/ERK pathway in an IKBKB-dependent manner in response to IL1B and TNF, but not insulin, leading to induction of lipolysis. Plays a role in the cell cycle. Isoform 1 shows some transforming activity, although it is much weaker than that of the activated oncogenic variant. |
| Cellular Location | Cytoplasm |
| Tissue Location | Expressed in several normal tissues and human tumor-derived cell lines |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Mitogen-activated protein kinase (MAPK) signaling cascades include MAPK or extracellular signal-regulated kinase (ERK), MAPK kinase (MKK or MEK), and MAPK kinase kinase (MAPKKK or MEKK). MAPKK kinase/MEKK phosphorylates and activates its downstream protein kinase, MAPK kinase/MEK, which in turn activates MAPK. The kinases of these signaling cascades are highly conserved, and homologs exist in yeast, Drosophila, and mammalian cells. MEKK8 is able to activate NF-kappa-B 1 by stimulating proteasome-mediated proteolysis of NF-kappa-B 1/p105. The protein appears to play an important role in the cell cycle. This cytoplasmic protein is expressed in several normal tissues and human tumor-derived cell lines. The 58 kDa form is activated specifically during the S and G2/M phases of the cell cycle. The longer form undergoes phosphorylation on Ser residues mainly, and the shorter form on both Ser and Thr residues.
REFERENCES
Sanchez-Gongora, E., et al., J. Biol. Chem. 275(40):31379-31386 (2000).
Aoki, M., et al., J. Biol. Chem. 268(30):22723-22732 (1993).
Chan, A.M., et al., Oncogene 8(5):1329-1333 (1993).
Miyoshi, J., et al., Mol. Cell. Biol. 11(8):4088-4096 (1991).
Aoki, M., et al., Oncogene 6(9):1515-1519 (1991).
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