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p38 alpha/MAPK14  Protein, Antibody, ELISA Kit, cDNA Clone

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Expression host: Baculovirus-Insect Cells  
10081-H08B-50
10081-H08B-20
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20 µg 
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Expression host: Baculovirus-Insect Cells  
10081-H07B-50
10081-H07B-20
50 µg 
20 µg 
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p38 alpha/MAPK14 Related Area

p38 alpha/MAPK14 Related Protein, Antibody, cDNA Gene, and ELISA Kits

p38 alpha/MAPK14 Summary & Protein Information

p38 alpha/MAPK14 Background

Gene Summary: The protein encoded by MAPK14 gene is a member of the MAP kinase family. MAPK14 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 MAPK14 gene encoding distinct isoforms have been reported. [provided by RefSeq, Jul 2008]
General information above from NCBI
Catalytic activity: ATP + a protein = ADP + a phosphoprotein.
Cofactor: Name=Mg(2+); Xref=ChEBI:CHEBI:18420; Evidence={ECO:0000269|PubMed:10838079};
Enzyme regulation: ENZYME REGULATION: Activated by cell stresses such as DNA damage, heat shock, osmotic shock, anisomycin and sodium arsenite, as well as pro-inflammatory stimuli such as bacterial lipopolysaccharide (LPS) and interleukin-1. Activation occurs through dual phosphorylation of Thr-180 and Tyr-182 by either of two dual specificity kinases, MAP2K3/MKK3 or MAP2K6/MKK6, and potentially also MAP2K4/MKK4, as well as by TAB1-mediated autophosphorylation. MAPK14 phosphorylated on both Thr-180 and Tyr-182 is 10-20-fold more active than MAPK14 phosphorylated only on Thr-180, whereas MAPK14 phosphorylated on Tyr-182 alone is inactive. whereas Thr-180 is necessary for catalysis, Tyr-182 may be required for auto-activation and substrate recognition. Phosphorylated at Tyr-323 by ZAP70 in an alternative activation pathway in response to TCR signaling in T-cells. This alternative pathway is inhibited by GADD45A. Inhibited by dual specificity phosphatases, such as DUSP1, DUSP10, and DUSP16. Specifically inhibited by the binding of pyridinyl-imidazole compounds, which are cytokine-suppressive anti-inflammatory drugs (CSAID). Isoform Mxi2 is 100-fold less sensitive to these agents than the other isoforms and is not inhibited by DUSP1. Isoform Exip is not activated by MAP2K6. SB203580 is an inhibitor of MAPK14. {ECO:0000269|PubMed:10391943, ECO:0000269|PubMed:10838079, ECO:0000269|PubMed:11278799, ECO:0000269|PubMed:11359773, ECO:0000269|PubMed:11847341, ECO:0000269|PubMed:11866441, ECO:0000269|PubMed:11896401, ECO:0000269|PubMed:12482439, ECO:0000269|PubMed:14561090, ECO:0000269|PubMed:14726206, ECO:0000269|PubMed:15735648, ECO:0000269|PubMed:15735649, ECO:0000269|PubMed:15837335, ECO:0000269|PubMed:16169718, ECO:0000269|PubMed:17003045, ECO:0000269|PubMed:7535770, ECO:0000269|PubMed:8622669, ECO:0000269|PubMed:9430721}.
Subunit structure: Binds to a kinase interaction motif within the protein tyrosine phosphatase, PTPRR (By similarity). This interaction retains MAPK14 in the cytoplasm and prevents nuclear accumulation (By similarity). Interacts with SPAG9 and GADD45A (By similarity). Interacts with CDC25B, CDC25C, DUSP1, DUSP10, DUSP16, NP60, SUPT20H and TAB1. Interacts with casein kinase II subunits CSNK2A1 and CSNK2B. {ECO:0000250, ECO:0000269|PubMed:10391943, ECO:0000269|PubMed:10747897, ECO:0000269|PubMed:11010976, ECO:0000269|PubMed:11278799, ECO:0000269|PubMed:11333986, ECO:0000269|PubMed:11359773, ECO:0000269|PubMed:11847341, ECO:0000269|PubMed:12897767, ECO:0000269|PubMed:15658854, ECO:0000269|PubMed:15735649, ECO:0000269|PubMed:16342939, ECO:0000269|PubMed:16352664, ECO:0000269|PubMed:16751104, ECO:0000269|PubMed:17255097, ECO:0000269|PubMed:20188673, ECO:0000269|PubMed:9792677}.
Domain: The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.
Subcellular location: Cytoplasm. Nucleus.
Tissue specificity: Brain, heart, placenta, pancreas and skeletal muscle. Expressed to a lesser extent in lung, liver and kidney.
Post-translational: Dually phosphorylated on Thr-180 and Tyr-182 by the MAP2Ks MAP2K3/MKK3, MAP2K4/MKK4 and MAP2K6/MKK6 in response to inflammatory citokines, environmental stress or growth factors, which activates the enzyme. Dual phosphorylation can also be mediated by TAB1-mediated autophosphorylation. TCR engagement in T-cells also leads to Tyr-323 phosphorylation by ZAP70. Dephosphorylated and inactivated by DUPS1, DUSP10 and DUSP16. {ECO:0000269|PubMed:11010976, ECO:0000269|PubMed:15735648, ECO:0000269|PubMed:17724032, ECO:0000269|PubMed:7535770, ECO:0000269|PubMed:8622669}.; Acetylated at Lys-53 and Lys-152 by KAT2B and EP300. Acetylation at Lys-53 increases the affinity for ATP and enhances kinase activity. Lys-53 and Lys-152 are deacetylated by HDAC3. {ECO:0000269|PubMed:21444723}.; Ubiquitinated. Ubiquitination leads to degradation by the proteasome pathway. {ECO:0000269|PubMed:17724032}.
Sequence similarity: Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily. {ECO:0000305}.; Contains 1 protein kinase domain. {ECO:0000255|PROSITE-ProRule:PRU00159}.
General information above from UniProt

MAPK14 contains 1 protein kinase domain and belongs to 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. MAPK14 can be detected in brain, heart, placenta, pancreas and skeletal muscle and it is expressed to a lesser extent in lung, liver and kidney. MAPK14 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 MAPK14. The substrates of p38 alpha include transcription regulator ATF2, MEF2C, and MAX, cell cycle regulator CDC25B, and tumor suppressor p53, which suggest the roles of p38 alpha in stress related transcription and cell cycle regulation, as well as in genotoxic stress response. In respond to activation by environmental stress, pro-inflammatory cytokines and lipopolysaccharide, MAPK14 phosphorylates a number of transcription factors, such as ELK1 and ATF2 and several downstream kinases, such as MAPKAPK2 and MAPKAPK5. MAPK14 plays a critical role in the production of some cytokines, for example IL-6. It may play a role in stabilization of EPO mRNA during hypoxic stress. Isoform Mxi2 activation is stimulated by mitogens and oxidative stress and only poorly phosphorylates ELK1 and ATF2.

p38 alpha/MAPK14 Alternative Name

p38,RK,CSBP,EXIP,Mxi2,CSBP1,CSBP2,CSPB1,PRKM14,PRKM15,SAPK2A,p38ALPHA, [homo-sapiens]
p38,CSBP1,CSBP2,CSPB1,EXIP,MAPK14,Mxi2,p38ALPHA,PRKM14,PRKM15,RK,RP1-179N16.5,SAPK2A, [human]
Crk1,Csbp1,CSBP2,Mapk14,MGC102436,Mxi2,p38,p38a,p38alpha,p38-alpha,p38MAPK,PRKM14,PRKM15,RP24-137E7.1, [mouse]
p38,Crk1,Mxi2,p38a,CSBP2,Csbp1,PRKM14,PRKM15,p38MAPK,p38alpha,p38-alpha, [mus-musculus]
CRK1,Csbp1,Csbp2,CSPB1,Exip,Hog,Mxi2,p38,p38alpha,p38Hog,Prkm14,Prkm15,RK,Sapk2A, [Rat]

p38 alpha/MAPK14 Related Studies

  • Luo X, et al. (2011) Study on p38 mitogen activated protein kinase in vascular endothelial cells dysfunction in preeclampsia. Zhonghua Fu Chan Ke Za Zhi. 46(1):36-40.
  • Park CH, et al. (2011) Epidermal growth factor-induced matrix metalloproteinase-1 expression is negatively regulated by p38 MAPK in human skin fibroblasts. J Dermatol Sci. 64(2):134-41.
  • Lee JY, et al. (2011) Curcumin induces EGFR degradation in lung adenocarcinoma and modulates p38 activation in intestine: the versatile adjuvant for gefitinib therapy. PLoS One. 6(8):e23756.
  • Riis JL, et al. (2011) CCL27 expression is regulated by both p38 MAPK and IKKβ signalling pathways. Cytokine. 56(3):699-707.
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