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。
JNK2 (MAPK9) Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | P45984 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 48139 Da |
| Antigen Region | 349-379 aa |
| Gene ID | 5601 |
|---|---|
| Other Names | Mitogen-activated protein kinase 9, MAP kinase 9, MAPK 9, JNK-55, Stress-activated protein kinase 1a, SAPK1a, Stress-activated protein kinase JNK2, c-Jun N-terminal kinase 2, MAPK9, JNK2, PRKM9, SAPK1A |
| Target/Specificity | This JNK2 (MAPK9) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 349-379 amino acids from the C-terminal region of human JNK2 (MAPK9). |
| 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 | JNK2 (MAPK9) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | MAPK9 |
|---|---|
| Synonyms | JNK2, PRKM9, SAPK1A |
| Function | Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death (PubMed:10376527, PubMed:15805466, PubMed:17525747, PubMed:19675674, PubMed:20595622, PubMed:21364637, PubMed:22441692, PubMed:34048572). Extracellular stimuli such as pro- inflammatory cytokines or physical stress stimulate the stress- activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK9/JNK2 (PubMed:10376527, PubMed:15805466, PubMed:17525747, PubMed:19675674, PubMed:20595622, PubMed:21364637, PubMed:22441692, PubMed:34048572). In turn, MAPK9/JNK2 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity (PubMed:10376527). In response to oxidative or ribotoxic stresses, inhibits rRNA synthesis by phosphorylating and inactivating the RNA polymerase 1-specific transcription initiation factor RRN3 (PubMed:15805466). Promotes stressed cell apoptosis by phosphorylating key regulatory factors including TP53 and YAP1 (PubMed:17525747, PubMed:21364637). In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells (PubMed:19290929). Upon T-cell receptor (TCR) stimulation, is activated by CARMA1, BCL10, MAP2K7 and MAP3K7/TAK1 to regulate JUN protein levels (PubMed:19290929). Plays an important role in the osmotic stress- induced epithelial tight-junctions disruption (PubMed:20595622). When activated, promotes beta-catenin/CTNNB1 degradation and inhibits the canonical Wnt signaling pathway (PubMed:19675674). Also participates in neurite growth in spiral ganglion neurons (By similarity). Phosphorylates the CLOCK-BMAL1 heterodimer and plays a role in the regulation of the circadian clock (PubMed:22441692). Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteasomal degradation (By similarity). Phosphorylates ALKBH5 in response to reactive oxygen species (ROS), promoting ALKBH5 sumoylation and inactivation (PubMed:34048572). |
| Cellular Location | Cytoplasm. Nucleus. Note=Colocalizes with POU5F1 in the nucleus. {ECO:0000250|UniProtKB:Q9WTU6} |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
JNK2 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2 and thus regulates AP-1 transcriptional activity. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells. JNK2 isoforms display different binding patterns: alpha-1 and alpha-2 preferentially bind to c-Jun, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 alpha-2, and JUND binds only weakly to it. JNK2 is activated by threonine and tyrosine phosphorylation by either of two dual specificity kinases, MAP2K4 and MAP2K7. It is inhibited by dual specificity phosphatases, such as DUSP1. The protein has been shown to bind to at least three scaffolding proteins, MAPK8IP1/JIP-1, MAPK8IP2/JIP-2 and MAPK8IP3/JIP-3/JSAP1. These proteins also bind other components of the JNK signaling pathway
REFERENCES
Gupta, S., et al., EMBO J. 15(11):2760-2770 (1996).
Sluss, H.K., et al., Mol. Cell. Biol. 14(12):8376-8384 (1994).
Kallunki, T., et al., Genes Dev. 8(24):2996-3007 (1994).
Fleming, Y., et al., Biochem. J. 352 Pt 1, 145-154 (2000).
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