Mitogen-activated protein kinase phosphatase-1: a critical phosphatase manipulating mitogen-activated protein kinase signaling in cardiovascular disease (review)
- PMID: 25695424
- DOI: 10.3892/ijmm.2015.2104
Mitogen-activated protein kinase phosphatase-1: a critical phosphatase manipulating mitogen-activated protein kinase signaling in cardiovascular disease (review)
Abstract
Mitogen-activated protein kinase (MAPK) cascades are important players in the overall representation of cellular signal transduction pathways, and the deregulation of MAPKs is involved in a variety of diseases. The activation of MAPK signals occurs through phosphorylation by MAPK kinases at conserved threonine and tyrosine (Thr-Xaa-Tyr) residues. The mitogen-activated protein kinase phosphatases (MKPs) are a major part of the dual-specificity family of phosphatases and specifically inactivate MAPKs by dephosphorylating both phosphotyrosine and phosphoserine/phosphothreonine residues within the one substrate. MAPKs binding to MKPs can enhance MKP stability and activity, providing an important negative-feedback control mechanism that limits the MAPK cascades. In recent years, accumulating and compelling evidence from studies mainly employing cultured cells and mouse models has suggested that the archetypal MKP family member, MKP-1, plays a pivotal role in cardiovascular disease as a major negative modulator of MAPK signaling pathways. In the present review, we summarize the current knowledge on the pathological properties and the regulation of MKP-1 in cardiovascular disease, which may provide valuable therapeutic options.
Similar articles
-
Catalytic activation of mitogen-activated protein (MAP) kinase phosphatase-1 by binding to p38 MAP kinase: critical role of the p38 C-terminal domain in its negative regulation.Biochem J. 2000 Nov 15;352 Pt 1(Pt 1):155-63. Biochem J. 2000. PMID: 11062068 Free PMC article.
-
Mitogen-activated protein kinase phosphatase (MKP)-1 in immunology, physiology, and disease.Life Sci. 2012 Feb 13;90(7-8):237-48. doi: 10.1016/j.lfs.2011.11.017. Epub 2011 Dec 13. Life Sci. 2012. PMID: 22197448 Free PMC article. Review.
-
CD40-modulated dual-specificity phosphatases MAPK phosphatase (MKP)-1 and MKP-3 reciprocally regulate Leishmania major infection.J Immunol. 2011 May 15;186(10):5863-72. doi: 10.4049/jimmunol.1003957. Epub 2011 Apr 6. J Immunol. 2011. PMID: 21471446
-
Diversity and specificity of the mitogen-activated protein kinase phosphatase-1 functions.Cell Mol Life Sci. 2013 Jan;70(2):223-37. doi: 10.1007/s00018-012-1041-2. Epub 2012 Jun 14. Cell Mol Life Sci. 2013. PMID: 22695679 Free PMC article. Review.
-
Mitogen-activated protein (MAP) kinase/MAP kinase phosphatase regulation: roles in cell growth, death, and cancer.Pharmacol Rev. 2008 Sep;60(3):261-310. doi: 10.1124/pr.107.00106. Pharmacol Rev. 2008. PMID: 18922965 Review.
Cited by
-
Dual-Specificity Phosphatases in Neuroblastoma Cell Growth and Differentiation.Int J Mol Sci. 2019 Mar 7;20(5):1170. doi: 10.3390/ijms20051170. Int J Mol Sci. 2019. PMID: 30866462 Free PMC article. Review.
-
Characterizing how probiotic Lactobacillus reuteri 6475 and lactobacillic acid mediate suppression of osteoclast differentiation.Bone Rep. 2019 Nov 2;11:100227. doi: 10.1016/j.bonr.2019.100227. eCollection 2019 Dec. Bone Rep. 2019. PMID: 31763377 Free PMC article.
-
Regulation of mitogen-activated protein kinase by protein kinase C and mitogen-activated protein kinase phosphatase-1 in vascular smooth muscle.Am J Physiol Cell Physiol. 2016 Jun 1;310(11):C921-30. doi: 10.1152/ajpcell.00311.2015. Epub 2016 Apr 6. Am J Physiol Cell Physiol. 2016. PMID: 27053523 Free PMC article.
-
Cardiac resynchronization therapy reduces expression of inflammation-promoting genes related to interleukin-1β in heart failure.Cardiovasc Res. 2020 Jun 1;116(7):1311-1322. doi: 10.1093/cvr/cvz232. Cardiovasc Res. 2020. PMID: 31612215 Free PMC article.
-
Mechanical stretching of pulmonary vein stimulates matrix metalloproteinase-9 and transforming growth factor-β1 through stretch-activated channel/MAPK pathways in pulmonary hypertension due to left heart disease model rats.PLoS One. 2020 Sep 3;15(9):e0235824. doi: 10.1371/journal.pone.0235824. eCollection 2020. PLoS One. 2020. PMID: 32881898 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous
