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Metformin sensitizes arsenic trioxide to suppress intrahepatic cholangiocarcinoma via the regulation of AMPK/p38 MAPK-ERK3/mTORC1 pathways. ERK3 is a newfound potential prognostic predictor and a tumor suppressor in ICC.
Study revealed a post-translational regulation of TDP2 activity and discovered a new role of ERK3 in increasing cancer cells' DNA damage response and chemoresistance to Top2 inhibitors.
MAPK6 could rescue the cell growth induced by miR499a and HBV
ERK3 regulates endothelial cell migration, proliferation and tube formation by upregulating SRC-3/SP-1-mediated VEGFR2 expression.
These findings further expand distinct roles of cyclin D3 and suggest the potential activity of ERK3 in cell proliferation.
Cdc14A forms a stable complex with atypical mitogen-activated protein kinase Erk3 in human cells independent of its intrinsic phosphatase activity but mediated by its regulatory C-terminal domain.
identify the Erk3 protein as a novel class I Pak substrate and further suggest a role for Pak kinase activity in atypical MAPK signaling.
A previously unknown role for ERK3 in promoting lung cancer cell invasiveness by phosphorylating SRC-3 and regulating SRC-3 proinvasive activity by site-specific phosphorylation.
ERK3 biological activity is regulated by its cellular abundance through the control of protein stability
Data show that extracellular signal-regulated kinase 3 (ERK3) is conjugated to ubiquitin via its free NH(2) terminus, and that N-terminal tags stabilize expression of p21 but not that of substrates ubiquitinated on internal lysine residues.
Extracellular signal-regulated kinase-3 (ERK3/MAPK6) is highly expressed in response to BRAF signaling.
Data show that extracellular-regulated kinase 3 (ERK3) specifically interacts with the MAPK-activated protein kinase 5 (MK5 or PRAK) in vitro and in vivo.
Results demonstrate a specific interaction between extracellular signal-regulated kinase 3 (ERK3) and mitogen-activated protein kinase-activated protein kinase-5 (MK5).
p38gamma MAP kinase (SAPK3/p38gamma) was shown to catalyse phosphorylation of SAP97.
Results show that Cdo is important for full Abl kinase activity, and Abl is necessary for full activation of p38 MAPK, during myogenic differentiation.
The Arabidopsis MKK4/MKK5-MPK6 cascade is an important player in the maternal control of embryogenesis.
abscisic acid and jasmonate mediate inactivation of the immune-associated MAP kinases (MAPKs), MPK3 and MPK6, in Arabidopsis thaliana ABA induced expression of genes encoding the protein phosphatases 2C (PP2Cs), HAI1, HAI2, and HAI3 through ABF/AREB transcription factors
Proteome changes associated with MPK4 and MPK6 deficiency in Arabidopsis roots.
Results suggest that these mutants can be used to analyze the specific biological functions of MAP kinase 6 (MPK6).
These data highlight MPK6 and MKP1 as components of an L-Glutamate pathway linking the auxin response, and cell division for primary root growth.
Genetic and biochemical evidences not only show that MEK1-MPK6 cascade, AtRBOHD/F-dependent H2O2 and NIA1-dependent NO are all involved in dark-induced stomatal closure in Arabidopsis, also indicate that MEK1-MPK6 cascade functions via working downstream of H2O2 and upstream of NO.
that MPK3/MPK6 phosphorylate and destabilize ICE1, which negatively regulates CBF expression and freezing tolerance in plants
BASL polarization leads to elevated nuclear MPK6 signaling and lowered SPCH abundance in one of the two daughter cells. Therefore, two daughter cells are differentiated by BASL polarity-mediated differential suppression of SPCH, which may provide developmental plasticity in plant stem cell asymmetric cell division.
results indicated that AIK1-MKK5-MPK6 functions in ABA responses and requires ABA-responsive gene expression to regulate ABA-inhibited root growth and cell division. The ABA signaling pathway regulates this MAPK cascade.
MPK6 role in ultraviolet induced stomatal closure
Study propose that the pathogen-responsive MPK3/MPK6 cascade and ABA are two essential signaling pathways that control, respectively, the organic acid metabolism and ion channels, two main branches of osmotic regulation in guard cells that function interdependently to control stomatal opening/closure.
MPK6-mediated regulation of MYB15 plays an important role in cold stress signaling in Arabidopsis.
Data report that MPK3/MPK6 and their substrate ERF6 promote the biosynthesis of IGSs and the conversion of I3G to 4MI3G, a target of PEN2/PEN3-dependent chemical defenses in plant immunity.
Data show that the protein kinases MPK3 and MPK6 can both interact with SPOROCYTELESS/NOZZLE (SPL) in vitro and in vivo and can phosphorylate the SPL protein in vitro.
AIK1-MKK5-MPK6 cascade functions in the abscisic acid regulation of primary root growth and stomatal response.
A novel mechanism for PIN1 phosphorylation involving MKK7 and MPK6 in shoot branching regulation in Arabidopsis.
MKK4, MKK5, MKK7, and MKK9, are responsible for the activation of MPK3 and MPK6 by melatonin, indicating that melatonin-mediated innate immunity is triggered by MAPK signaling through MKK4/5/7/9-MPK3/6 cascades.
Phosphatase AP2C1, as well as AP2C1-targeted MPK3 and MPK6, are important regulators of plant-nematode interaction, where the co-ordinated action of these signalling components ensures the timely activation of plant defence.
Mitogen-activated protein kinase 6 (MPK6) promoted C-terminal end of ORE3/EIN2 (CEND cleavage and nuclear translocation. Nuclear CEND accumulated ETHYLENE INSENSITIVE3 (EIN3), a transcription factor that accelerates MeJA-induced leaf senescence.
Results demonstrated the contribution of MPK3 and MPK6 to riboflavin-induced resistance.
The protein encoded by this gene is a member of the Ser/Thr protein kinase family, and is most closely related to mitogen-activated protein kinases (MAP kinases). MAP kinases also known as extracellular signal-regulated kinases (ERKs), are activated through protein phosphorylation cascades and act as integration points for multiple biochemical signals. This kinase is localized in the nucleus, and has been reported to be activated in fibroblasts upon treatment with serum or phorbol esters.
, MAP kinase 6
, MAP kinase isoform p97
, MAPK 6
, extracellular signal-regulated kinase 3
, extracellular signal-regulated kinase, p97
, protein kinase, mitogen-activated 5
, protein kinase, mitogen-activated 6
, Erk-3 related
, mitogen activated protein kinase 4
, mitogen activated protein kinase 6
, protein kinase, mitogen activated kinase 4
, extracellular related kinase 3
, mitogen-activated protein kinase 6