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  4. Recombinant Mouse Mitogen-activated protein kinase 14 (Mapk14)

Recombinant Mouse Mitogen-activated protein kinase 14 (Mapk14)

  • 货号：
    CSB-YP013453MO
  • 规格：
  • 来源：
    Yeast
  • 其他：
  • 货号：
    CSB-EP013453MO-B
  • 规格：
  • 来源：
    E.coli
  • 共轭：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 货号：
    CSB-BP013453MO
  • 规格：
  • 来源：
    Baculovirus
  • 其他：
  • 货号：
    CSB-MP013453MO
  • 规格：
  • 来源：
    Mammalian cell
  • 其他：

产品详情

  • 纯度：
    >85% (SDS-PAGE)
  • 基因名：
  • Uniprot No.：
  • 别名：
    Mapk14; Crk1; Csbp1; Csbp2Mitogen-activated protein kinase 14; MAP kinase 14; MAPK 14; EC 2.7.11.24; CRK1; Mitogen-activated protein kinase p38 alpha; MAP kinase p38 alpha
  • 种属：
    Mus musculus (Mouse)
  • 蛋白长度：
    Full Length of Mature Protein
  • 表达区域：
    2-360
  • 氨基酸序列
    SQERPTFYR QELNKTIWEV PERYQNLSPV GSGAYGSVCA AFDTKTGHRV AVKKLSRPFQ SIIHAKRTYR ELRLLKHMKH ENVIGLLDVF TPARSLEEFN DVYLVTHLMG ADLNNIVKCQ KLTDDHVQFL IYQILRGLKY IHSADIIHRD LKPSNLAVNE DCELKILDFG LARHTDDEMT GYVATRWYRA PEIMLNWMHY NQTVDIWSVG CIMAELLTGR TLFPGTDHID QLKLILRLVG TPGAELLKKI SSESARNYIQ SLAQMPKMNF ANVFIGANPL AVDLLEKMLV LDSDKRITAA QALAHAYFAQ YHDPDDEPVA DPYDQSFESR DLLIDEWKSL TYDEVISFVP PPLDQEEMES
  • 蛋白标签：
    Tag type will be determined during the manufacturing process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 产品提供形式：
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 复溶：
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK14 is one of the four p38 MAPKs which play an important role in the cascades of cellular responses evoked by extracellular stimuli such as proinflammatory cytokines or physical stress leading to direct activation of transcription factors. Accordingly, p38 MAPKs phosphorylate a broad range of proteins and it has been estimated that they may have approximately 200 to 300 substrates each. Some of the targets are downstream kinases which are activated through phosphorylation and further phosphorylate additional targets. RPS6KA5/MSK1 and RPS6KA4/MSK2 can directly phosphorylate and activate transcription factors such as CREB1, ATF1, the NF-kappa-B isoform RELA/NFKB3, STAT1 and STAT3, but can also phosphorylate histone H3 and the nucleosomal protein HMGN1. RPS6KA5/MSK1 and RPS6KA4/MSK2 play important roles in the rapid induction of immediate-early genes in response to stress or mitogenic stimuli, either by inducing chromatin remodeling or by recruiting the transcription machinery. On the other hand, two other kinase targets, MAPKAPK2/MK2 and MAPKAPK3/MK3, participate in the control of gene expression mostly at the post-transcriptional level, by phosphorylating ZFP36 (tristetraprolin) and ELAVL1, and by regulating EEF2K, which is important for the elongation of mRNA during translation. MKNK1/MNK1 and MKNK2/MNK2, two other kinases activated by p38 MAPKs, regulate protein synthesis by phosphorylating the initiation factor EIF4E2. MAPK14 interacts also with casein kinase II, leading to its activation through autophosphorylation and further phosphorylation of TP53/p53. In the cytoplasm, the p38 MAPK pathway is an important regulator of protein turnover. For example, CFLAR is an inhibitor of TNF-induced apoptosis whose proteasome-mediated degradation is regulated by p38 MAPK phosphorylation. In a similar way, MAPK14 phosphorylates the ubiquitin ligase SIAH2, regulating its activity towards EGLN3. MAPK14 may also inhibit the lysosomal degradation pathway of autophagy by interfering with the intracellular trafficking of the transmembrane protein ATG9. Another function of MAPK14 is to regulate the endocytosis of membrane receptors by different mechanisms that impinge on the small GTPase RAB5A. In addition, clathrin-mediated EGFR internalization induced by inflammatory cytokines and UV irradiation depends on MAPK14-mediated phosphorylation of EGFR itself as well as of RAB5A effectors. Ectodomain shedding of transmembrane proteins is regulated by p38 MAPKs as well. In response to inflammatory stimuli, p38 MAPKs phosphorylate the membrane-associated metalloprotease ADAM17. Such phosphorylation is required for ADAM17-mediated ectodomain shedding of TGF-alpha family ligands, which results in the activation of EGFR signaling and cell proliferation. Another p38 MAPK substrate is FGFR1. FGFR1 can be translocated from the extracellular space into the cytosol and nucleus of target cells, and regulates processes such as rRNA synthesis and cell growth. FGFR1 translocation requires p38 MAPK activation. In the nucleus, many transcription factors are phosphorylated and activated by p38 MAPKs in response to different stimuli. Classical examples include ATF1, ATF2, ATF6, ELK1, PTPRH, DDIT3, TP53/p53 and MEF2C and MEF2A. The p38 MAPKs are emerging as important modulators of gene expression by regulating chromatin modifiers and remodelers. The promoters of several genes involved in the inflammatory response, such as IL6, IL8 and IL12B, display a p38 MAPK-dependent enrichment of histone H3 phosphorylation on 'Ser-10' (H3S10ph) in LPS-stimulated myeloid cells. This phosphorylation enhances the accessibility of the cryptic NF-kappa-B-binding sites marking promoters for increased NF-kappa-B recruitment. Phosphorylates CDC25B and CDC25C which is required for binding to 14-3-3 proteins and leads to initiation of a G2 delay after ultraviolet radiation. Phosphorylates TIAR following DNA damage, releasing TIAR from GADD45A mRNA and preventing mRNA degradation. The p38 MAPKs may also have kinase-independent roles, which are thought to be due to the binding to targets in the absence of phosphorylation. Protein O-Glc-N-acylation catalyzed by the OGT is regulated by MAPK14, and, although OGT does not seem to be phosphorylated by MAPK14, their interaction increases upon MAPK14 activation induced by glucose deprivation. This interaction may regulate OGT activity by recruiting it to specific targets such as neurofilament H, stimulating its O-Glc-N-acylation. Required in mid-fetal development for the growth of embryo-derived blood vessels in the labyrinth layer of the placenta. Also plays an essential role in developmental and stress-induced erythropoiesis, through regulation of EPO gene expression. Phosphorylates S100A9 at 'Thr-113'.
  • 基因功能参考文献：
    1. results define a key role for p38alpha in luminal progenitor cell fate that affects mammary tumor formation. PMID: 29290625
    2. Lysosomal p38 MAPK directly phosphorylates LAMP2A at T211 and T213, which causes its membrane accumulation and active conformational change, activating chaperone-mediated autophagy. PMID: 29176575
    3. p38-mediated phosphorylation at threonine 367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis. PMID: 30022044
    4. Results implicate neuronal p38alpha signaling in the synaptic plasticity dysfunction and memory impairment observed in 5XFAD mice, by regulating both amyloid-beta deposition in the brain and the relay of this accumulation to mount an inflammatory response, which leads to the cognitive deficits. PMID: 28361984
    5. These findings uncovered the molecular mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinates osteoclastogenesis and osteoblastogenesis. PMID: 28382965
    6. Praja1 promotes skeletal myogenesis through degradation of EZH2 upon p38alpha activation. PMID: 28067271
    7. These results suggested that the thrombinstimulated synthesis of IL6 was limited by HSP90 in osteoblasts, and that the effects of HSP90 were exerted at the point between Rhokinase and p38 MAPK. PMID: 30066835
    8. Overall, the s showed that CCN1 increased IL-1beta production via p38 MAPK signaling, indicating a role for CCN1 protein in regulating inflammation in psoriasis. PMID: 28266627
    9. we have identified novel interaction between p38 MAPK and Runx2 enhances Runx2 transactivity, thus promoting vascular smooth muscle cells calcification PMID: 29495001
    10. p38alpha MAPK maintains the expression of antioxidant genes in liver of young animals via NF-kappaBeta under basal conditions, whereas its long-term deficiency triggers compensatory up-regulation of antioxidant enzymes through NF-kappaBeta. PMID: 29567616
    11. the present findings suggested that artesunate may exert protective effects against cerebral ischemia/reperfusion injury through the suppression of oxidative and inflammatory processes, via activating Nrf2 and downregulating ROSdependent p38 MAPK in mice. PMID: 29512760
    12. Results show that the p38 MAPK signaling pathway could regulate mitochondria Abeta internalization by manipulating the expression of alpha7nAChR. Pretreatment of alpha7nAChR agonist could attenuate these biochemical changes which are tightly associated with Abeta1-42 induced apoptosis. Suggesting there is an endogenous, previously unrecognized cholinergic mechanism to control mitochondria functions and their apoptotic ... PMID: 29128415
    13. Prdx1 knockout can aggravate the oxidative stress and lung injury by increasing the level of Reactive Oxygen Species (ROS), and also activate P38/JNK signaling pathway. PMID: 28485790
    14. P38 kinase role in the inflammatory pain.CXCL13, upregulated by peripheral inflammation, acts on CXCR5 on dorsal root ganglia neurons and activates p38, which increases Nav1.8 current density and further contributes to the maintenance of inflammatory pain. PMID: 27708397
    15. these findings indicate that BMS309403 reduces fatty acid-induced ER stress-associated inflammation in skeletal muscle by reducing p38 MAPK activation. PMID: 29550588
    16. report insulin-like growth factor-II binding protein 1 (IGF2BP1) as a novel interacting partner of p38 MAPK. PMID: 28497370
    17. These results were supported by the opposite outcomes observed for cells treated with A779 or DX600. Therefore, it was concluded that the ACE2-Ang(17)-Mas axis significantly inhibits pancreatitis by inhibition of the p38 MAPK/NF-kappaB signaling pathway PMID: 29138810
    18. results suggest that c-Jun, p38 MAPK, PIK3CA/Akt, and GSK3 signaling involved in the effect of miR-203 on the proliferation of hepatocellular carcinoma cells. PMID: 28887744
    19. MAPK in, and found that p38alpha deficiency causes Th1 cells to hyperproliferate via the Mnk1/eIF4E pathway PMID: 28611474
    20. B7-H1 suppresses p38 MAPK activation by sequestering DNA-PKcs in order to preserve T cell survival PMID: 27824138
    21. increased in lentivirus vector thioredoxin interacting protein (LV-GFP-TXNIP) cells. PMID: 29169415
    22. Our data demonstrated that p38 MAPK may be a potential therapeutic target for hypertension-related cognitive dysfunction. PMID: 27283322
    23. Endogenous hydrogen sulfide-mediated MAPK inhibition preserves endothelial function through TXNIP signaling. PMID: 28669627
    24. Our key findings provide novel insights into the mechanism of action of heterotrimeric complex (PKCdelta-TIRAP-p38) in proinflammatory cytokine expression, which controls the development of the inflammatory trigger in stimulated macrophages. PMID: 28528205
    25. CXCL13 acts on CXCR5 to increase p38 activation and further contributes to the pathogenesis of orofacial neuropathic pain PMID: 28155010
    26. p38 role in the Helicobacter pylori podocyte infiltration PMID: 28803254
    27. Our data suggest that rCC16 suppresses LPS-mediated inflammatory mediator TNF-alpha, IL-6, and IL-8 production by inactivating NF-kappaB and p38 MAPK but not AP-1 in RAW264.7 cells. PMID: 28338974
    28. high fat diet (HFD) and zinc deficiency synergistically induce obesity-related cardiac hypertrophy (ORCH), by increasing oxidative stress-mediated activation of BCL10/CARD9/p38 MAPK signalling. Zinc supplement ameliorates ORCH through activation of metallothionein to repress oxidative stress-activated BCL10 expression and p38 MAPK activation. PMID: 28158919
    29. involvement of CacyBP/SIP in the regulation of p38 kinase activity, in addition to that of ERK1/2, might point to the function of CacyBP/SIP in pro-survival and pro-apoptotic pathways. PMID: 28283909
    30. Macrophage p38alpha-deficient mice had decreased mortality and GalN/TNF-alpha-induced liver injury apoptosis, less apoptosis, accelerated regeneration, decreased granulocyte recruitment, monocytes infiltration, and cytokine production after GalN/TNF-alpha treatment. Mechanistically, p38 signaling was activated by lipopolysaccharide/interferon-gamma treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibi PMID: 29052963
    31. Overall, our results provide the first evidence that HDAC6 is capable of inducing expression of pro-inflammatory genes by regulating the ROS-MAPK-NF-kappaB/AP-1 pathways and serves as a molecular target for inflammation. PMID: 27208785
    32. YZH-106 induced p38 MAPK and ERK1/2 phosphorylation, which led to the activation of erythroid 2-related factor 2 (Nrf2) that up-regulated heme oxygenase-1 (HO-1) expression in addition to other genes. PMID: 27107768
    33. Trehalose may rescue against insulin resistance-induced myocardial contractile defect and apoptosis, via autophagy associated with dephosphorylation of p38 MAPK and Foxo1 without affecting phosphorylation of Akt. PMID: 27363949
    34. SPAK plays a pathogenic role in IgA nephropathy through the activation of NF-kappaB/MAPK signaling pathway. PMID: 27519267
    35. cyclophilin-dependent isomerisation of p38MAPK is an important novel mechanism in regulating p38MAPK phosphorylation and functions. PMID: 27233083
    36. findings identify p38alpha MAPK as a key component of PTH signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity PMID: 26643857
    37. p38alpha serves as a critical regulator of platelet activation and potential indicator of highly thrombotic lesions and no-reflow in ST-elevation myocardial infarction. PMID: 28982666
    38. Blockade of TRPV1, through genetic deletion or systemic or intra-nucleus accumbens (NAc) pharmacological means, inhibited morphine-induced CPP in mice. In addition, p38 MAPK inhibition blocked development of morphine conditioned place preference (CPP) as well. Moreover, blockade of either NAc p38 MAPK or TRPV1 dampened protein expression levels of p-p38 MAPK, AC1, and p-NF-kappaB which are normally induced by morphine ... PMID: 28734766
    39. Results demonstrate that in vivo attenuation of p38alpha activity slows age-associated decline in dentate gyrus neurogenesis and associated cognitive function. Aged DN-p38alphaAF/+ mice produce more adult-born neurons than wildtype littermates, suggesting that p38alpha negatively contributes to age-dependent decline in neurogenesis that underlies the age-dependent decline in context discrimination. PMID: 27765672
    40. bn1 expression is induced during myoblast differentiation, in a p38 MAP kinase- and MyoD- dependent manner. RNAi-mediated depletion of drebrin, or treatment with a chemical drebrin inhibitor, resulted in a similar phenotype in myoblasts: defective differentiation, with low levels of early and late differentiation markers and inefficient production of myofibers. PMID: 28865032
    41. In vitro, SCF induced the phosphorylation of p38 MAPK and cofilin, leading to the migration of cardiac stem cells. PMID: 28986094
    42. Park2 deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 kinase dependent inhibition of autophagy and mitochondrial function. PMID: 28086194
    43. Mechanistic experiments revealed that treatment with cryptotanshinone activated AMPKalpha and p38-MAPK via their phosphorylation: the two major signaling pathways regulating energy metabolism. PMID: 28807877
    44. This is the first report proclaiming that the ESAT-6 regulates Prdx-1 which is involved in the increase of mycobacterial uptake and survival. The intermediate mechanisms involve the increased Prdx-1 production in macrophages through the activation of p38 and NRF-2 dependent signaling. PMID: 29032183
    45. Data suggest that activity of neuronal enzymes Akt1 and p38Mapk can be modulated by dietary factors; here, subchronic administration of ascorbic acid (a common antioxidant, antidepressant dietary supplement) at 1 mg/kg increases Akt1 phosphorylation in cerebral cortex of mice and decreases hippocampal p38Mapk phosphorylation. (Akt1 = thymoma viral proto-oncogene 1; p38Mapk = p38 MAP kinase) PMID: 27721116
    46. S. aureus evades phagophores and prevents further degradation by a MAPK14/p38alpha MAP kinase-mediated blockade of autophagy. PMID: 27629870
    47. The anti-inflammatory functions of p38 MAPK in macrophages are critically dependent on production of IL-10. PMID: 28877953
    48. this study shows that peripheral deletion of CD8 T cells requires p38 MAPK in cross-presenting dendritic cells PMID: 28864471
    49. p38MAPK/MK2 phosphorylation of RIPK1 is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction. PMID: 28920954
    50. Data suggest that Mapk14/p38alpha is activated and forms cystine disulfide-bound heterodimer with Map2k3/Mkk3 in cardiomyocytes and isolated hearts during oxidative stress. (Mapk14, mitogen-activated protein kinase 14; Mkk3 = mitogen-activated protein kinase kinase 3) PMID: 28739872

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  • 亚细胞定位：
    Cytoplasm. Nucleus.
  • 蛋白家族：
    Protein kinase superfamily, CMGC Ser/Thr protein kinase family, MAP kinase subfamily
  • 组织特异性：
    Macrophages, monocytes, T- and B-lymphocytes. Isoform 2 is specifically expressed in kidney and liver.
  • 数据库链接：

    KEGG: mmu:26416

    STRING: 10090.ENSMUSP00000004990

    UniGene: Mm.311337