Formalin-fixed, paraffin-embedded human Colon stained with MAPK14 Mouse Monoclonal Antibody (CPTC-MAPK14-1).

Analysis of Protein Array containing more than 19,000 full-length human proteins using MAPK14 Mouse Monoclonal Antibody (CPTC-MAPK14-1). Z- and S- Score: The Z-score represents the strength of a signal that a monoclonal antibody (Monoclonal Antibody) (in combination with a fluorescently-tagged anti-IgG secondary antibody) produces when binding to a particular protein on the HuProtTM array. Z-scores are described in units of standard deviations (SD's) above the mean value of all signals generated on that array. If targets on HuProtTM are arranged in descending order of the Z-score, the S-score is the difference (also in units of SD's) between the Z-score. S-score therefore represents the relative target specificity of a Monoclonal Antibody to its intended target. A Monoclonal Antibody is considered to specific to its intended target, if the Monoclonal Antibody has an S-score of at least 2.5. For example, if a Monoclonal Antibody binds to protein X with a Z-score of 43 and to protein Y with a Z-score of 14, then the S-score for the binding of that Monoclonal Antibody to protein X is equal to 29.

Printable Datasheet

MAPK14 [CPTC-MAPK14-1]

Name: MAPK14
SKU: 1432-MSM1
Availability: InStock

Monoclonals Mouse Monoclonals Primary Antibodies

Summary

The protein encoded by this gene 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 environmental stresses and proinflammatory cytokines. The activation requires its phosphorylation by MAP kinase kinases (MKKs), or its autophosphorylation triggered by the interaction of MAP3K7IP1/TAB1 protein with this kinase. The substrates of this kinase include transcription regulator ATF2, MEF2C, and MAX, cell cycle regulator CDC25B, and tumor suppressor p53, which suggest the roles of this kinase in stress related transcription and cell cycle regulation, as well as in genotoxic stress response. Four alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported. It has been implicated in various cancer pathologies and depending on the context, can facilitate or interfere with tumor development, and therefore has immense potential therapeutic interest.

Product Properties & Targets

Host

Mouse

Applications

Immunohistochemistry

Species Reactivity

Human

Research Areas

Autophagy, Cardiovascular

Isotype

IgG1

Cellular Localization

Cytoplasm, Nucleus

Light Chain

Kappa

Gene Name

MAPK14

Positive Control

C6, Jurkat, NIH/3T3 or HeLa cell lysate.

Immunogen

Recombinant human full length protein

Alternate Names

Mitogen-activated protein kinase 14, Cytokine suppressive anti-inflammatory drug-binding protein, MAP kinase MXI2, MAX-interacting protein 2, Mitogen-activated protein kinase p38 alpha, Stress-activated protein kinase 2a, CSBP, CSBP1, CSBP2, CSPB1, MXI2, SAPK2A, p38, PRKM15

Database Links

Entrez Gene ID

1432

Unigene

485233

SwissProt

Q16539

Additional Information

Clone

CPTC-MAPK14-1

Human Gene Symbol

MAPK14

Chromosome Location

6p21.31

Mol. Weight of Antigen

41.6kDa

Functions

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 pro-inflammatory 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. Isoform MXI2 activation is stimulated by mitogens and oxidative stress and only poorly phosphorylates ELK1 and ATF2. Isoform EXIP may play a role in the early onset of apoptosis. Phosphorylates S100A9 at 'Thr-113'.
(Microbial infection) Activated by phosphorylation by M.tuberculosis EsxA in T-cells leading to inhibition of IFN-gamma production; phosphorylation is apparent within 15 minutes and is inhibited by kinase-specific inhibitors SB203580 and siRNA (PubMed:21586573).

Known Applications & Suggested Dilutions

Immunohistochemistry (Formalin-fixed) (1-2ug/ml for 30 min at RT)(Staining of formalin-fixed tissues requires heating tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 45 min at 95&degC followed by cooling at RT for 20 minutes)
Optimal dilution for a specific application should be determined.

Key References

Igea, Ana, and Angel R. Nebreda. Cancer Research, American Association for Cancer Research, 1 Oct. 2015.

PubMed Links

Storage & Stability

Antibody with azide - store at 2 to 8°C. Antibody without azide - store at -20 to -80°C. Antibody is stable for 24 months. Non-hazardous. No MSDS required.

Limitations

This antibody is available for research use only and is not approved for use in diagnosis.

Supplied as

200ug/ml of Ab Purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA & azide at 1.0mg/ml.

Warranty

There are no warranties, expressed or implied, which extend beyond this description. Company is not liable for any personal injury or economic loss resulting from this product.

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