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Mitogen-activated protein kinase 7

ERK5, Mitogen-Activated Protein Kinase 7, BMK1, extracellular signal-regulated kinase 5
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 specifically activated by mitogen-activated protein kinase kinase 5 (MAP2K5/MEK5). It is involved in the downstream signaling processes of various receptor molecules including receptor type kinases, and G protein-coupled receptors. In response to extracelluar signals, this kinase translocates to cell nucleus, where it regulates gene expression by phosphorylating, and activating different transcription factors. Four alternatively spliced transcript variants of this gene encoding two distinct isoforms have been reported. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MAPK, ERK1, MEK5, ERK, p38
Papers on ERK5
Involvement of Extracellular Signal-regulated Kinase 5 in Kinin B1 Receptor Up-regulation in Isolated Human Umbilical Vein.
New
Rothlin et al., Buenos Aires, Argentina. In J Pharmacol Exp Ther, Feb 2016
The aim of this study was to evaluate the involvement of extracellular signal-regulated kinase 5 (ERK5), p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) on kinin B1 receptor up-regulation process in HUV, employing functional and biochemical methods.
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
New
Miyazono et al., Uppsala, Sweden. In Stem Cell Reports, Feb 2016
In contrast, the MEK5-ERK5 pathway mediates BMP-4-induced self-renewal of mESCs by inducing Klf2, a critical factor for the ground state pluripotency.
Disturbed flow-induced endothelial pro-atherogenic signaling via regulating post-translational modifications and epigenetic events.
New
Abe et al., Houston, United States. In Antioxid Redox Signal, Jan 2016
Activation of PKCζ and p90RSK, SUMOylation of ERK5 and p53, and DNA hypermethylation are uniquely induced by d-flow, but not by s-flow.
ERK5 induces ankrd1 for catecholamine biosynthesis and homeostasis in adrenal medullary cells.
New
Nakahata et al., Sendai, Japan. In Cell Signal, Jan 2016
In our previous study, we demonstrated that both ERK5 and ERK1/2 were responsible for neurite outgrowth and tyrosine hydroxylase (TH) expression in rat pheochromocytoma cells (PC12) (J Biol Chem 284, 23,564-23,573, 2009).
ERK5 Mediated Signalling in Diabetic Retinopathy.
Review
Chakrabarti et al., London, Canada. In Med Hypothesis Discov Innov Ophthalmol, 2014
Extracellular signal-regulated kinase 5 (ERK5), also known as big mitogen-activated protein kinase 1 (BMK1), is a member of mitogen-activated protein kinases (MAPK) family.
Application of the ERK signaling pathway inhibitor PD98059 in long-term in vivo experiments.
Tang et al., Changsha, China. In Genet Mol Res, 2014
The corresponding treatments were administered to each experimental group over the course of four weeks, after which, total ERK1/2 and ERK5 protein levels, protein phosphorylation, and gene expression were measured in myocardial tissues.
Novel mechanisms of endothelial mechanotransduction.
Review
Berk et al., Rochester, United States. In Arterioscler Thromb Vasc Biol, 2014
We will focus on 5 mechanosensitive pathways: mitogen-activated protein kinases/extracellular signal-regulated kinase 5/Kruppel-like factor 2 signaling, extracellular signal-regulated kinase/peroxisome proliferator-activated receptor signaling, and mechanosignaling pathways involving SUMOylation, protein kinase C-ζ, and p90 ribosomal S6 kinase.
Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives.
Review
Agostini et al., United States. In Pharmacol Ther, 2014
The extensively studied MAPKs ERK1/2, p38, JNK, and ERK5, demonstrate unique intracellular signaling mechanisms, responding to a myriad of mitogens and stressors and influencing the signaling of cardiac development, metabolism, performance, and pathogenesis.
[Research progress on MAPK signal pathway in the pathogenesis of osteoarthritis].
Review
Sui et al., In Zhongguo Gu Shang, 2014
MAPKs in eukaryotes include p38, ERK, JNK and ERK5, etc.
Mitogen-activated protein kinase signal transduction in solid tumors.
Review
Wang et al., Nanchang, China. In Asian Pac J Cancer Prev, 2013
There are 5 main subgroups manipulating by a set of sequential actions: ERK(ERK1/ ERK2), c-Jun N(JNK/SAPK), p38 MAPK(p38α, p38β, p38γ and p38δ), and ERK3/ ERK4/ ERK5.
Progesterone increases the release of brain-derived neurotrophic factor from glia via progesterone receptor membrane component 1 (Pgrmc1)-dependent ERK5 signaling.
GeneRIF
Singh et al., Fort Worth, United States. In Endocrinology, 2012
Data describe that P4 elicits an increase in BDNF release from glia via a Pgrmc1-induced ERK5 signaling mechanism and identify Pgrmc1 as a potential therapeutic target for future hormone-based drug development.
ERK5 protein promotes, whereas MEK1 protein differentially regulates, the Toll-like receptor 2 protein-dependent activation of human endothelial cells and monocytes.
GeneRIF
Hellman et al., San Francisco, United States. In J Biol Chem, 2012
study newly identifies ERK5 as a key regulator of TLR2 signaling in EC and monocytes and indicates that there are fundamental differences in TLR signaling pathways between EC and monocytes
Inducible and conditional deletion of extracellular signal-regulated kinase 5 disrupts adult hippocampal neurogenesis.
GeneRIF
Xia et al., Seattle, United States. In J Biol Chem, 2012
Data suggest ERK5 signaling as a critical regulator of adult hippocampal neurogenesis.
6 Paths of ERK5 signaling pathway regulate hepatocyte proliferation in rat liver regeneration.
GeneRIF
Xu et al., Xinxiang, China. In Indian J Biochem Biophys, 2012
The study shows that 22 genes and 6 paths of ERK5 signaling pathway participate in regulating proliferation of hepatocytes in rat liver regeneration.
Inhibition of adult neurogenesis by inducible and targeted deletion of ERK5 mitogen-activated protein kinase specifically in adult neurogenic regions impairs contextual fear extinction and remote fear memory.
GeneRIF
Xia et al., Seattle, United States. In J Neurosci, 2012
ERK5 MAP kinase displays a novel signaling pathway regulating adult neurogenesis in the dentate gyrus and demonstrates a causal relationship between ERK5-regulated adult neurogenesis and the expression of remote memory.
Mpk1 MAPK association with the Paf1 complex blocks Sen1-mediated premature transcription termination.
Impact
Levin et al., Boston, United States. In Cell, 2011
Finally, we demonstrate that this mechanism is conserved in an interaction between the human ERK5 MAPK and human Paf1.
Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.
Review
Impact
Wang et al., Los Angeles, United States. In Physiol Rev, 2010
The four best characterized MAPK subfamilies, ERK1/2, JNK, p38, and ERK5, are the targets of pharmacological and genetic manipulations to uncover their roles in cardiac development, function, and diseases.
Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein.
Impact
GeneRIF
Lee et al., Los Angeles, United States. In Cancer Cell, 2010
We found that BMK1 interacted with promyelocytic leukemia protein (PML), and inhibited its tumor-suppressor function through phosphorylation.
The protein kinase A anchoring protein mAKAP coordinates two integrated cAMP effector pathways.
Impact
Scott et al., Portland, United States. In Nature, 2005
Anchored PKA stimulates PDE4D3 to reduce local cAMP concentrations, whereas an mAKAP-associated ERK5 kinase module suppresses PDE4D3.
Bmk1/Erk5 is required for cell proliferation induced by epidermal growth factor.
Impact
Lee et al., Los Angeles, United States. In Nature, 1998
Big MAP kinase (Bmk1), also known as Erk5, is a member of the MAP kinase family that is activated in cells in response to oxidative stress, hyperosmolarity and treatment with serum.
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