JNK3 protein

    • 货号：YD0060
    • 应用：WB;SDS-PAGE
    • 种属：Human
      • 基因名称：
      • MAPK10
      • 蛋白名称：
      • JNK3 protein
      • 序列：
      • Amino acid: 21-110, with his-MBP tag.
      • Human Gene Id：
      • 5602
      • Human Swiss Prot No：
      • P53779
      • Mouse Swiss Prot No：
      • Q61831
      • 组成：
      • Liquid in PBS
      • 来源：
      • E.coli
      • 稀释：
      • WB 1:500-2000
      • 浓度：
      • SDS-PAGE >90%
      • 储存：
      • -20°C/6 month,-80°C for long storage
      • 其他名称：
      • Mitogen-activated protein kinase 10 (MAP kinase 10) (MAPK 10) (EC 2.7.11.24) (MAP kinase p49 3F12) (Stress-activated protein kinase 1b) (SAPK1b) (Stress-activated protein kinase JNK3) (c-Jun N-terminal kinase 3)
      • 背景：
      • alternative products:A similar low level of binding to substrates is observed for isoform alpha-1 and isoform alpha-2. However, there is no correlation between binding and phosphorylation, which is achieved about at the same efficiency by all isoforms,catalytic activity:ATP + a protein = ADP + a phosphoprotein.,caution:The sequence shown here is derived from an Ensembl automatic analysis pipeline and should be considered as preliminary data.,cofactor:Magnesium.,disease:A chromosomal rearrangement involving MAPK10 is a cause of epileptic encephalopathy Lennox-Gastaut type [MIM:606369]. Translocation t(Y;4)(q11.2;q21) which causes MAPK10 truncation. Epileptic encephalopathies of the Lennox-Gastaut group are childhood epileptic disorders characterized by severe psychomotor delay and seizures.,domain:The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.,enzyme regulation:Activated by threonine and tyrosine phosphorylation by two dual specificity kinases, MAP2K4 and MAP2K7. MAP2K7 phosphorylates MAPK10 on Thr-221 causing a conformational change and a large increase in Vmax. MAP2K4 then phosphorylates Tyr-223 resulting in a further increase in Vmax. Inhibited by dual specificity phosphatases, such as DUSP1. Inhibited by HDAC9.,function: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. Required for stress-induced neuronal apoptosis and the pathogenesis of glutamate excitotoxicity.,mass spectrometry: PubMed:10715136,PTM:Dually phosphorylated on Thr-221 and Tyr-223, which activates the enzyme. Weakly autophosphorylated on threonine and tyrosine residues in vitro.,similarity:Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.,similarity:Contains 1 protein kinase domain.,subunit:Interacts with MAPKBP1 (By similarity). 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. Interacts with HDAC9.,tissue specificity:Specific to a subset of neurons in the nervous system. Present in the hippocampus and areas, cerebellum, striatum, brain stem, and weakly in the spinal cord. Very weak expression in testis and kidney.,
      • 功能：
      • MAPKKK cascade, protein amino acid phosphorylation, phosphorus metabolic process, phosphate metabolic process,intracellular signaling cascade, protein kinase cascade, JNK cascade, phosphorylation, stress-activated protein kinase signaling pathway, cellular response to stress,
      • 细胞定位：
      • Cytoplasm . Membrane ; Lipid-anchor . Nucleus . Mitochondrion . Palmitoylation regulates MAPK10 trafficking to cytoskeleton. Recruited to the mitochondria in the presence of SARM1 (By similarity). .
      • 组织表达：
      • Specific to a subset of neurons in the nervous system. Present in the hippocampus and areas, cerebellum, striatum, brain stem, and weakly in the spinal cord. Very weak expression in testis and kidney.
      • 产品图片

      相关报价

      • 货号：
      • YD0060
      • 规格：
      • 100μg
      • 价格：
      • ¥2300
      • 货期：
      • 预计发货时间为
        2024-12-29
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