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Gene Review

Mapk14  -  mitogen activated protein kinase 14

Rattus norvegicus

Synonyms: CRK1, CSBP, CSPB1, Csbp1, Csbp2, ...
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Disease relevance of Mapk14

  • These studies demonstrate that an extremely typical physiological stress (hypoxia) causes selective activation of specific p38 signaling elements; and they also identify a downstream target of these pathways [1].
  • In contrast to our expectation, treatment with the NPC31169 resulted in worse renal function, more proteinuria, and more severe glomerulosclerosis and tubulointerstitial injury. p38 inhibition resulted in marked cell proliferation in RK rats, with more proliferating tubular cells, myofibroblasts, and macrophages [2].
  • To test the hypothesis that p38 mediates renal disease progression, we administered a novel p38 alpha inhibitor, NPC31169, to rats with remnant kidneys (RKs) [2].
  • Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis [3].
  • In progressive anti-GBM disease, p38 and JNK activation in podocytes, glomerular endothelial cells, infiltrating macrophages, T cells, and myofibroblasts suggests that both the p38 and JNK MAPK pathways are important in chronic inflammation and fibrosis [3].

Psychiatry related information on Mapk14

  • Differential activation of c-Jun N-terminal protein kinase and p38 in rat hippocampus and cerebellum after electroconvulsive shock [4].
  • The intra-CA1 infusion of SP600125, at a dose that in naïve animals significantly reduced the phosphorylation levels of c-Jun without affecting the activity of ERK1/2 or p38 MAPK, enhanced short-term memory (STM) but blocked long-term memory (LTM) formation and retrieval of an inhibitory avoidance learning task [5].
  • CONCLUSION: p38 MAPK plays an important role in the pressor response induced by central administration of IL-1 beta or footshock and change of motor activity after footshock in conscious rats [6].

High impact information on Mapk14

  • The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells [7].
  • In contrast, cardiac-specific p38alpha knockout mice show a 92.3% increase in neonatal cardiomyocyte mitoses [8].
  • Protection by DEJL peptide binding was observed in loops spanning beta7-beta8 and alphaD-alphaE in p38alpha and ERK2 [9].
  • Here we show that the p38 MAP kinase pathway, a parallel signaling cascade activated by distinct upstream kinases, mediates the induction of metabotropic glutamate receptor-dependent long-term depression at CA3-CA1 synapses [10].
  • Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in long-term potentiation at hippocampal CA3-CA1 synapses has been well described, relatively little is known about the importance of the p38 MAP kinase pathway in synaptic plasticity [10].

Chemical compound and disease context of Mapk14


Biological context of Mapk14


Anatomical context of Mapk14


Associations of Mapk14 with chemical compounds

  • We also examined the effect of Tyrphostin A46 (potent inhibitor of EGF-R and EGF-R kinase-dependent proliferation) on the above parameters [23].
  • Phosphorylation of serine 105 enhanced the transcriptional potency of GATA4, which was sensitive to U0126 (MEK1 inhibitor) but not SB202190 (p38 inhibitor) [24].
  • Whereas SB203580 inhibited endotoxin-induced NF-kappaB activation, pyrrolidine dithiocarbamate did not affect p38 phosphorylation in endotoxin-stimulated cells [25].
  • In this study, we found that endotoxin causes activation of mitogen-activated protein kinases (MAPKs) (extracellular signal-regulated protein kinase [ERK] 1 and 2, p38, and c-Jun NH2-terminal kinase [JNK]) and nuclear factor kappaB (NF-kappaB) and production of H(2)O(2) in culture-activated HSCs [25].
  • Thus, angiotensin II, by a mechanism that requires the participation of p38 MAPK, differentially regulates the expression of NF-kappaB-dependent genes in response to interleukin-1beta stimulation by controlling the duration of activation of ERK and NF-kappaB [26].

Physical interactions of Mapk14

  • Treatment with a p38 MAPK inhibitor, PD169316, or transfection with a dominant-negative p38 MAPK construct reversed the effect of CD or ceramide to stabilize COX-2 mRNA [27].
  • In this study, IFN-gamma enhancement of TNF-alpha-induced NF-kappaB binding affinity as well as p38 MAP kinase activation was observed [28].
  • The data seem to indicate that JNK and p38 MAPK activations are not necessarily coupled to DNA binding of AP-1, which can be either increased or inhibited when these kinases are activated [29].
  • More importantly, p38 kinase formed a complex with p53 after the treatment of CAPE for 0.5 hr [30].
  • Furthermore, our data clearly show that an accelerating AMPA receptor endocytosis by stimulating the formation of guanyl nucleotide dissociation inhibitor-Rab5 complex is a potential downstream processing of p38 MAPK activation to mediate DHPG-LTD [31].

Enzymatic interactions of Mapk14


Regulatory relationships of Mapk14


Other interactions of Mapk14

  • Stimulation with bFGF alone had no effect on the activity of either p38 or Akt but markedly enhanced p38 phosphorylation mediated by sst(2(a)) receptors, suggesting that a complex interplay exists between the transduction cascades activated by these distinct receptor types [16].
  • Mechanisms of endotoxin-induced NO, IL-6, and TNF-alpha production in activated rat hepatic stellate cells: role of p38 MAPK [25].
  • p38, a mitogen-activated protein kinase, is a major intracellular signaling molecule involved in inflammation [2].
  • Elevated levels of cyclooxygenase-2 in antigen-stimulated mast cells is associated with minimal activation of p38 mitogen-activated protein kinase [38].
  • Endothelin-1-specific activation of B-type natriuretic peptide gene via p38 mitogen-activated protein kinase and nuclear ETS factors [35].

Analytical, diagnostic and therapeutic context of Mapk14


  1. Selective activation of p38alpha and p38gamma by hypoxia. Role in regulation of cyclin D1 by hypoxia in PC12 cells. Conrad, P.W., Rust, R.T., Han, J., Millhorn, D.E., Beitner-Johnson, D. J. Biol. Chem. (1999) [Pubmed]
  2. Inhibition of p38 mitogen-activated protein kinase augments progression of remnant kidney model by activating the ERK pathway. Ohashi, R., Nakagawa, T., Watanabe, S., Kanellis, J., Almirez, R.G., Schreiner, G.F., Johnson, R.J. Am. J. Pathol. (2004) [Pubmed]
  3. Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis. Stambe, C., Atkins, R.C., Hill, P.A., Nikolic-Paterson, D.J. Kidney Int. (2003) [Pubmed]
  4. Differential activation of c-Jun N-terminal protein kinase and p38 in rat hippocampus and cerebellum after electroconvulsive shock. Oh, S.W., Ahn, Y.M., Kang, U.G., Kim, Y.S., Park, J.B. Neurosci. Lett. (1999) [Pubmed]
  5. Inhibition of hippocampal Jun N-terminal kinase enhances short-term memory but blocks long-term memory formation and retrieval of an inhibitory avoidance task. Bevilaqua, L.R., Kerr, D.S., Medina, J.H., Izquierdo, I., Cammarota, M. Eur. J. Neurosci. (2003) [Pubmed]
  6. p38 MAPK mediates cardiovascular and behavioral responses induced by central IL-1 beta and footshock in conscious rats. Zheng, R.M., Zou, C.J., Zhu, S.G. Acta Pharmacol. Sin. (2004) [Pubmed]
  7. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis. Xia, Z., Dickens, M., Raingeaud, J., Davis, R.J., Greenberg, M.E. Science (1995) [Pubmed]
  8. p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes. Engel, F.B., Schebesta, M., Duong, M.T., Lu, G., Ren, S., Madwed, J.B., Jiang, H., Wang, Y., Keating, M.T. Genes Dev. (2005) [Pubmed]
  9. Docking motif interactions in MAP kinases revealed by hydrogen exchange mass spectrometry. Lee, T., Hoofnagle, A.N., Kabuyama, Y., Stroud, J., Min, X., Goldsmith, E.J., Chen, L., Resing, K.A., Ahn, N.G. Mol. Cell (2004) [Pubmed]
  10. Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3-CA1 synapses. Bolshakov, V.Y., Carboni, L., Cobb, M.H., Siegelbaum, S.A., Belardetti, F. Nat. Neurosci. (2000) [Pubmed]
  11. Cyclooxygenase-2-dependent and thromboxane-dependent vascular and bronchial responses are regulated via p38 mitogen-activated protein kinase in control and endotoxin-primed rat lungs. Ermert, M., Kuttner, D., Eisenhardt, N., Dierkes, C., Seeger, W., Ermert, L. Lab. Invest. (2003) [Pubmed]
  12. Antihypertrophic effect of Na+/H+ exchanger isoform 1 inhibition is mediated by reduced mitogen-activated protein kinase activation secondary to improved mitochondrial integrity and decreased generation of mitochondrial-derived reactive oxygen species. Javadov, S., Baetz, D., Rajapurohitam, V., Zeidan, A., Kirshenbaum, L.A., Karmazyn, M. J. Pharmacol. Exp. Ther. (2006) [Pubmed]
  13. Inhibition of p38 mitogen-activated protein kinase interferes with cell shape changes and gene expression associated with Schwann cell myelination. Fragoso, G., Robertson, J., Athlan, E., Tam, E., Almazan, G., Mushynski, W.E. Exp. Neurol. (2003) [Pubmed]
  14. Role of ERK and p38 mitogen-activated protein kinase cascades in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide. Slomiany, B.L., Slomiany, A. IUBMB Life (2001) [Pubmed]
  15. Mitogen-activated protein kinases (p38 and c-Jun NH2-terminal kinase) are differentially regulated during cardiac volume and pressure overload hypertrophy. Sopontammarak, S., Aliharoob, A., Ocampo, C., Arcilla, R.A., Gupta, M.P., Gupta, M. Cell Biochem. Biophys. (2005) [Pubmed]
  16. Receptor isoforms mediate opposing proliferative effects through gbetagamma-activated p38 or Akt pathways. Sellers, L.A., Alderton, F., Carruthers, A.M., Schindler, M., Humphrey, P.P. Mol. Cell. Biol. (2000) [Pubmed]
  17. Role of MAP kinases and their cross-talk in TGF-beta1-induced apoptosis in FaO rat hepatoma cell line. Park, H.J., Kim, B.C., Kim, S.J., Choi, K.S. Hepatology (2002) [Pubmed]
  18. Extracellular signal-regulated kinase and p38 subgroups of mitogen-activated protein kinases regulate inducible nitric oxide synthase and tumor necrosis factor-alpha gene expression in endotoxin-stimulated primary glial cultures. Bhat, N.R., Zhang, P., Lee, J.C., Hogan, E.L. J. Neurosci. (1998) [Pubmed]
  19. CYP2E1 overexpression alters hepatocyte death from menadione and fatty acids by activation of ERK1/2 signaling. Schattenberg, J.M., Wang, Y., Rigoli, R.M., Koop, D.R., Czaja, M.J. Hepatology (2004) [Pubmed]
  20. Arachidonic acid inhibits the insulin induction of glucose-6-phosphate dehydrogenase via p38 MAP kinase. Talukdar, I., Szeszel-Fedorowicz, W., Salati, L.M. J. Biol. Chem. (2005) [Pubmed]
  21. A role for the extracellular signal-regulated kinase and p38 mitogen-activated protein kinases in interleukin-1 beta-stimulated delayed signal tranducer and activator of transcription 3 activation, atrial natriuretic factor expression, and cardiac myocyte morphology. Ng, D.C., Long, C.S., Bogoyevitch, M.A. J. Biol. Chem. (2001) [Pubmed]
  22. Gangliosides activate cultured rat brain microglia. Pyo, H., Joe, E., Jung, S., Lee, S.H., Jou, I. J. Biol. Chem. (1999) [Pubmed]
  23. Induction of mitogen-activated protein kinase signal transduction pathway during gastric ulcer healing in rats. Pai, R., Ohta, M., Itani, R.M., Sarfeh, I.J., Tarnawski, A.S. Gastroenterology (1998) [Pubmed]
  24. The transcription factor GATA4 is activated by extracellular signal-regulated kinase 1- and 2-mediated phosphorylation of serine 105 in cardiomyocytes. Liang, Q., Wiese, R.J., Bueno, O.F., Dai, Y.S., Markham, B.E., Molkentin, J.D. Mol. Cell. Biol. (2001) [Pubmed]
  25. Mechanisms of endotoxin-induced NO, IL-6, and TNF-alpha production in activated rat hepatic stellate cells: role of p38 MAPK. Thirunavukkarasu, C., Watkins, S.C., Gandhi, C.R. Hepatology (2006) [Pubmed]
  26. Angiotensin II differentially regulates interleukin-1-beta-inducible NO synthase (iNOS) and vascular cell adhesion molecule-1 (VCAM-1) expression: role of p38 MAPK. Jiang, B., Xu, S., Hou, X., Pimentel, D.R., Cohen, R.A. J. Biol. Chem. (2004) [Pubmed]
  27. Posttranscriptional regulation of cyclooxygenase-2 in rat intestinal epithelial cells. Zhang, Z., Sheng, H., Shao, J., Beauchamp, R.D., DuBois, R.N. Neoplasia (2000) [Pubmed]
  28. Blockade of p38 mitogen-activated protein kinase pathway inhibits interleukin-6 release and expression in primary neonatal cardiomyocytes. Chae, H., Lee, J., Byun, J., Jung, W., Kwak, Y., Chae, S., Kim, H. Res. Commun. Mol. Pathol. Pharmacol. (2001) [Pubmed]
  29. Influence of proteasome and redox state on heat shock-induced activation of stress kinases, AP-1 and HSF. Tacchini, L., Dansi, P., Matteucci, E., Bernelli-Zazzera, A., Desiderio, M.A. Biochim. Biophys. Acta (2001) [Pubmed]
  30. Involvement of tumor suppressor protein p53 and p38 MAPK in caffeic acid phenethyl ester-induced apoptosis of C6 glioma cells. Lee, Y.J., Kuo, H.C., Chu, C.Y., Wang, C.J., Lin, W.C., Tseng, T.H. Biochem. Pharmacol. (2003) [Pubmed]
  31. Rap1-induced p38 mitogen-activated protein kinase activation facilitates AMPA receptor trafficking via the GDI.Rab5 complex. Potential role in (S)-3,5-dihydroxyphenylglycene-induced long term depression. Huang, C.C., You, J.L., Wu, M.Y., Hsu, K.S. J. Biol. Chem. (2004) [Pubmed]
  32. Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by pro-inflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase. Ma, K.K., Ogawa, T., de Bold, A.J. J. Mol. Cell. Cardiol. (2004) [Pubmed]
  33. Mechanical stretch-induced apoptosis in smooth muscle cells is mediated by beta1-integrin signaling pathways. Wernig, F., Mayr, M., Xu, Q. Hypertension (2003) [Pubmed]
  34. Tyrosine phosphorylation of Vav stimulates IL-6 production in mast cells by a Rac/c-Jun N-terminal kinase-dependent pathway. Song, J.S., Haleem-Smith, H., Arudchandran, R., Gomez, J., Scott, P.M., Mill, J.F., Tan, T.H., Rivera, J. J. Immunol. (1999) [Pubmed]
  35. Endothelin-1-specific activation of B-type natriuretic peptide gene via p38 mitogen-activated protein kinase and nuclear ETS factors. Pikkarainen, S., Tokola, H., Kerkelä, R., Majalahti-Palviainen, T., Vuolteenaho, O., Ruskoaho, H. J. Biol. Chem. (2003) [Pubmed]
  36. Activation of signal transducers and activators of transcription by alpha(1A)-adrenergic receptor stimulation in PC12 cells. Zhong, H., Murphy, T.J., Minneman, K.P. Mol. Pharmacol. (2000) [Pubmed]
  37. Inhibition of p38 mitogen-activated protein kinase enhances adrenergic-stimulated arylalkylamine N-acetyltransferase activity in rat pinealocytes. Man, J.R., Rustaeus, S., Price, D.M., Chik, C.L., Ho, A.K. Endocrinology (2004) [Pubmed]
  38. Elevated levels of cyclooxygenase-2 in antigen-stimulated mast cells is associated with minimal activation of p38 mitogen-activated protein kinase. Hundley, T.R., Prasad, A.R., Beaven, M.A. J. Immunol. (2001) [Pubmed]
  39. ICAM-1-induced expression of proinflammatory cytokines in astrocytes: involvement of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase pathways. Lee, S.J., Drabik, K., Van Wagoner, N.J., Lee, S., Choi, C., Dong, Y., Benveniste, E.N. J. Immunol. (2000) [Pubmed]
  40. Regional myocardial ischemia-induced activation of MAPKs is associated with subcellular redistribution of caveolin and cholesterol. Ballard-Croft, C., Locklar, A.C., Kristo, G., Lasley, R.D. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  41. Sphingolipids differentially regulate mitogen-activated protein kinases and intracellular Ca2+ in vascular smooth muscle: effects on CREB activation. Mathieson, F.A., Nixon, G.F. Br. J. Pharmacol. (2006) [Pubmed]
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