FITC标记的氨基末端激酶1/3抗体
产品名称: FITC标记的氨基末端激酶1/3抗体
英文名称: Anti-JNK1 + JNK3/FITC
产品编号: HZ-20760R-FITC
产品价格: null
产品产地: 中国/上海
品牌商标: HZbscience
更新时间: 2023-08-17T10:24:20
使用范围: ICC=1:50-200 IF=1:50-200
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Rabbit Anti-JNK1 + JNK3/FITC Conjugated antibody
FITC标记的氨基末端激酶1/3抗体
英文名称 | Anti-JNK1 + JNK3/FITC |
中文名称 | FITC标记的氨基末端激酶1/3抗体 |
别 名 | JNK1 + JNK3; JNK1 + 3; JNK1+JNK3; JNK1/3; c Jun N terminal kinase 1; JNK1; JNK3; JAK 1A; JAK1A; JNK 1; JNK 46; JNK; JNK1A2; JNK21B1/2; MAPK 8; MAPK8; Mitogen activated protein kinase 8; PRKM 8; PRKM8; Protein kinase JNK1; SAPK 1; SAPK gamma; SAPK1; c-Jun; Stress activated protein kinase JNK1; Tyrosine protein kinase JAK1; MK08_HUMAN. |
规格价格 | 100ul/2980元 购买 大包装/询价 |
说 明 书 | 100ul |
研究领域 | 肿瘤 细胞生物 免疫学 信号转导 转录调节因子 激酶和磷酸酶 |
抗体来源 | Rabbit |
克隆类型 | Polyclonal |
交叉反应 | Human, Mouse, Rat, Chicken, Pig, Cow, Horse, Rabbit, Sheep, |
产品应用 | ICC=1:50-200 IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
分 子 量 | 42kDa |
性 状 | Lyophilized or Liquid |
浓 度 | 2mg/1ml |
免 疫 原 | KLH conjugated synthetic peptide derived from human JNK1 + JNK3 |
亚 型 | IgG |
纯化方法 | affinity purified by Protein A |
储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
产品介绍 | background: JNK1(MAPK8) is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various cell stimuli, and targets specific transcription factors, and thus mediates immediate-early gene expression in response to cell stimuli. The activation of this kinase by tumor-necrosis factor alpha (TNF-alpha) is found to be required for TNF-alpha induced apoptosis. This kinase is also involved in UV radiation induced apoptosis, which is thought to be related to cytochrome c-mediated cell death pathway. Studies of the mouse counterpart of this gene suggested that this kinase play a key role in T cell proliferation, apoptosis and differentiation. Four alternatively spliced transcript variants encoding distinct isoforms have been reported. JNK1 is activated by threonine and tyrosine phosphorylation by either of two dual specificity kinases, MAP2K4 and MAP2K7. The JNK pathway is critically involved in diabetes and levels are abnormally elevated in obesity. The cell-permeable JNK inhibitory peptide may have promise as a therapeutic agent for diabetes. Function: Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory 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 MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including p53/TP53 and Yes-associates protein YAP1. In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Contributes to the survival of erythroid cells by phosphorylating the antagonist of cell death BAD upon EPO stimulation. Mediates starvation-induced BCL2 phosphorylation, BCL2 dissociation from BECN1, and thus activation of autophagy. Phosphorylates STMN2 and hence regulates microtubule dynamics, controlling neurite elongation in cortical neurons. In the developing brain, through its cytoplasmic activity on STMN2, negatively regulates the rate of exit from multipolar stage and of radial migration from the ventricular zone. Phosphorylates several other substrates including heat shock factor protein 4 (HSF4), the deacetylase SIRT1, ELK1, or the E3 ligase ITCH. Subunit: Binds to at least four scaffolding proteins, MAPK8IP1/JIP-1, MAPK8IP2/JIP-2, MAPK8IP3/JIP-3/JSAP1 and SPAG9/MAPK8IP4/JIP-4. These proteins also bind other components of the JNK signaling pathway. Forms a complex with MAPK8IP1 and RGNEF. Interacts with TP53 and WWOX. Interacts with JAMP. Interacts with NFATC4. Interacts with MECOM; regulates JNK signaling. Interacts with PIN1; this interaction mediates MAPK8 conformational changes leading to the binding of MAPK8 to its substrates. Interacts (phosphorylated form) with NFE2; the interaction phosphorylates NFE2 in undifferentiated cells. Subcellular Location: Cytoplasm. Nucleus. Post-translational modifications: Phosphorylated by TAOK2. Dually phosphorylated on Thr-183 and Tyr-185 by MAP2K7 and MAP2K4, which activates the enzyme. Similarity: Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily. Contains 1 protein kinase domain. Database links: Entrez Gene: 5599 Human Entrez Gene: 5601 Human Entrez Gene: 26419 Mouse Entrez Gene: 26420 Mouse Omim: 601158 Human Omim: 602896 Human SwissProt: P45983 Human SwissProt: P45984 Human SwissProt: Q91Y86 Mouse SwissProt: Q9WTU6 Mouse Unigene: 138211 Human Unigene: 348446 Human Unigene: 21495 Mouse Unigene: 68933 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications |
JNK1(MAPK8)是MAP激酶家族的成员。MAP激酶作为多种生化信号的整合点,参与细胞增殖、分化、转录调控和发育等多种细胞过程。这种激酶被各种细胞刺激激活,并且靶向特定的转录因子,从而响应于细胞刺激而介导即时早期基因表达。肿瘤坏死因子α(TNF-α)激活这种激酶是TNF-α诱导细胞凋亡所必需的。该激酶还参与UV辐射诱导的细胞凋亡,被认为与细胞色素c介导的细胞死亡途径有关。该基因的小鼠对应物的研究表明,该激酶在T细胞增殖、凋亡和分化中起关键作用。报道了四种编码不同亚型的剪接转录变体。JNK1通过苏氨酸和酪氨酸磷酸化被两种双重特异性激酶MAP2K4和MAP2K7激活。JNK途径与糖尿病密切相关,肥胖水平异常升高。细胞可渗透的JNK抑制肽可能具有作为糖尿病治疗剂的前景。