| 產(chǎn)品編號(hào) | bs-1977R-Gold |
| 英文名稱1 | Rabbit Anti-MEK4/Gold Conjugated antibody |
| 中文名稱 | 膠體金標(biāo)記的絲裂原活化蛋白激酶激酶4抗體 |
| 別 名 | c Jun N terminal kinase kinase 1; c-Jun N-terminal kinase kinase 1; c-Jun N-terminal kinase kinase 1; Dual specificity mitogen activated protein kinase kinase 4; Dual specificity mitogen activated protein kinase kinase 4; Dual specificity mitogen-activated protein kinase kinase 4; JNK activated kinase 1; JNK Activated Kinase 1; JNK activating kinase 1; JNK activating kinase 1; JNK-activating kinase 1; JNKK 1; JNKK; JNKK; JNKK-1; JNKK-1; JNKK1; JNKK1; MAP kinase kinase 4; MAP kinase kinase 4; MAP2K4; MAPK / ERK kinase 4; MAPK / ERK kinase 4; MAPK ERK kinase 4; MAPK/ERK kinase 4; MAPKK 4; MAPKK 4; MAPKK-4; MAPKK-4; MAPKK4; MAPKK4; MEK 4; MEK 4; MEK-4; MEK-4; MEK4; Mitogen Activated Protein Kinase Kinase 4; MKK 4; MKK-4; MKK-4; MKK4; MKK4; MP2K4_HUMAN; PRKMK 4; PRKMK 4; PRKMK-4; PRKMK-4; PRKMK4; PRKMK4; SAPK / ERK kinase 1; SAPK / ERK kinase 1; SAPK ERK kinase 1; SAPK/ERK Kinase 1; SEK 1; SEK1; SEK1; SERK 1; SERK-1; SERK-1; SERK1; SERK1. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買 大包裝/詢價(jià) |
| 說(shuō) 明 書 | 100ul（10nm 15nm 35nm） |
| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 免疫學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 轉(zhuǎn)錄調(diào)節(jié)因子 激酶和磷酸酶 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human, Mouse, Rat, Dog, Cow, ) |
| 產(chǎn)品應(yīng)用 | IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 44kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 0.4mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human MKK4/MAP2K4 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300. |
| 保存條件 | Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles. |
| 產(chǎn)品介紹 |
background: This gene encodes a member of the mitogen-activated protein kinase (MAPK) family. Members of this family 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. They form a three-tiered signaling module composed of MAPKKKs, MAPKKs, and MAPKs. This protein is phosphorylated at serine and threonine residues by MAPKKKs and subsequently phosphorylates downstream MAPK targets at threonine and tyrosine residues. A similar protein in mouse has been reported to play a role in liver organogenesis. A pseudogene of this gene is located on the long arm of chromosome X. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2013] 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 proinflammatory 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. Subunit: Interacts with SPAG9 (By similarity). Interacts (via its D domain) with its substrates MAPK8/JNK1, MAPK9/JNK2, MAPK10/JNK3, MAPK11 and MAPK14. Interacts (via its DVD domain) with MAP3Ks activators like MAP3K1/MEKK1 and MAP3K11/MLK3. Interacts with ARRB1, ARRB2 and MAPK8IP3/JIP3. Subcellular Location: Cytoplasm. Nucleus. Tissue Specificity: Abundant expression is seen in the skeletal muscle. It is also widely expressed in other tissues. Post-translational modifications: Activated by phosphorylation on Ser-257 and Thr-261 by MAP kinase kinase kinases (MAP3Ks). Similarity: Belongs to the protein kinase superfamily. STE Ser/Thr protein kinase family. MAP kinase kinase subfamily. Contains 1 protein kinase domain. Database links: Entrez Gene: 6416 Human Entrez Gene: 26398 Mouse Entrez Gene: 399471 Xenopus laevis Omim: 601335 Human SwissProt: P45985 Human SwissProt: P47809 Mouse Unigene: 514681 Human Unigene: 412922 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 研究發(fā)現(xiàn)---絲裂原活化蛋白激酶激酶4（MKK4）信號(hào)途徑對(duì)肝臟再生具有重要的意義 肝臟是人體最大的內(nèi)臟器官，承擔(dān)著數(shù)百種功能，包括產(chǎn)生蛋白質(zhì)與凝血因子，以及促進(jìn)消化與能量釋放等。肝功能衰竭（Liver Failure）是由于肝細(xì)胞受到廣泛嚴(yán)重的損害，機(jī)體代謝功能發(fā)生嚴(yán)重紊亂而出現(xiàn)的臨床綜合征。肝衰竭發(fā)生于許多嚴(yán)重的肝臟疾病過(guò)程中，癥候險(xiǎn)惡，預(yù)后多不良。 近日，俄勒岡健康與科學(xué)大學(xué)，加州大學(xué)舊金山分校的研究人員介紹了近期一項(xiàng)可用于治療肝功能衰竭的新成果：研究人員發(fā)現(xiàn)了著名信號(hào)途徑JNK中的一種激酶——絲裂原活化蛋白激酶激酶4（MKK4）對(duì)肝臟再生具有重要的意義。相關(guān)文章刊登在了近期出版的《細(xì)胞》（Cell）雜志上。 研究顯示肝細(xì)胞質(zhì)量是通過(guò)肝細(xì)胞死亡和再生之間的平衡來(lái)維系的，急性和慢性肝功能損傷會(huì)失去這種再生能力。因此圍繞肝臟再生，科學(xué)家們展開了許多研究。在這篇文章中，研究人員發(fā)現(xiàn)了一種潛在的藥物靶標(biāo)，能增強(qiáng)肝細(xì)胞增殖，促進(jìn)肝臟再生，防止肝功能衰竭。 研究人員研發(fā)了一種能有效篩選動(dòng)物疾病模型中調(diào)控肝臟再生基因的方法，他們?cè)趯?duì)小鼠肝臟中數(shù)百個(gè)基因的表達(dá)進(jìn)行干擾分析后，發(fā)現(xiàn)在急性和慢性肝損傷后，抑制MKK4基因能有效增加肝細(xì)胞的生成和生存，從而促進(jìn)肝臟修復(fù)，增加小鼠的壽命。而且這種MKK4基因的抑制，也會(huì)提高培養(yǎng)基中肝細(xì)胞長(zhǎng)時(shí)間存活的數(shù)量，這為促進(jìn)肝病患者肝移植提供了一種新方法。 研究人員表示，這一成果指出MKK4也許能作為一種促進(jìn)肝細(xì)胞增殖，肝臟再生的藥物靶標(biāo)，這為研發(fā)新型肝病治療方法提出了新思路。 此前，這組研究人員通過(guò)觀察成體干細(xì)胞標(biāo)記物L(fēng)gr5，以及響應(yīng)生長(zhǎng)因子Wnt的細(xì)胞生長(zhǎng)，第一次鑒別出了小腸和結(jié)腸中的干細(xì)胞。并推測(cè)，Lgr5的獨(dú)特表達(dá)模式也可以用于標(biāo)記其他成體組織，包括肝臟中的干細(xì)胞。并在這一方法的基礎(chǔ)上進(jìn)行了改良，利用新方法，研究人員發(fā)現(xiàn)Wnt誘導(dǎo)Lgr5表達(dá)不僅可以標(biāo)記肝臟中的干細(xì)胞生成，還可以確定一種在肝損傷時(shí)變得活躍的干細(xì)胞。 研究人員希望能大規(guī)模的擴(kuò)增這些肝細(xì)胞，隨后將它們轉(zhuǎn)化為肝細(xì)胞，用于治療人類慢性肝病。 |
