Affinage

Showing MAPK7 — ERK5 is a alias.

MAPK7

Mitogen-activated protein kinase 7 · UniProt Q13164

Length
816 aa
Mass
88.4 kDa
Annotated
2026-06-10
100 papers in source corpus 45 papers cited in narrative 45 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAPK7 (ERK5/BMK1) is a dual-function MAP kinase that couples growth-factor, mechanical, and oxidative-stress signaling to transcriptional programs governing cell proliferation, survival, and vascular/endothelial homeostasis (PMID:7646528, PMID:9790194, PMID:15085193). It carries an N-terminal kinase domain bearing a TEY dual-phosphorylation motif and a distinctive large C-terminal region that contains a transcriptional activation domain, a nuclear localization signal, and a MEF2-interaction module, the latter required for ERK5 to bind, phosphorylate, and coactivate MEF2 transcription factors (PMID:7646528, PMID:9753748, PMID:11046135, PMID:11139578). Activation flows through a dedicated module in which MEKK2 or MEKK3 (cell-type-specifically) feed into MEK5, which dually phosphorylates ERK5, with WNK1 acting upstream of the MEKKs and diverse inputs (EGF/NGF receptor tyrosine kinases, RET-Y1062, ALK via PI3K-AKT, oncogenic BRAF, fluid shear stress via PIEZO1/CaMKII, and H2O2 via c-Src) converging on this cascade (PMID:9790194, PMID:10593883, PMID:11073940, PMID:11237712, PMID:14681216, PMID:25351247, PMID:29483645, PMID:35883633). Nuclear translocation and transcriptional output are gated by multiple post-translational events distinct from TEY phosphorylation: C-terminal autophosphorylation, CDK1-mediated mitotic phosphorylation, SUMOylation at Lys6/Lys22, and ERK1/2-mediated Thr732 phosphorylation (PMID:11139578, PMID:20736311, PMID:25689862, PMID:32209980). In addition to MEF2 and the Ets factor Sap1a, ERK5 phosphorylates SGK (Ser78), Bad (Ser112/136), PML, and p90 RSK, and engages NF-κB, promoting proliferation and survival while inhibiting apoptosis (PMID:10473620, PMID:11118448, PMID:11254654, PMID:14670836, PMID:16626623, PMID:20832753). Genetic ablation establishes ERK5 as essential for endothelial integrity, where its loss causes vascular leakage, endothelial apoptosis, and lethality partly through deregulation of MEF2C (PMID:15085193), and it drives macrophage efferocytosis, EMT suppression, and tumor proliferation (PMID:20832753, PMID:22282661, PMID:25001623). A critical reinterpretation of this biology comes from work showing that ERK5 kinase inhibitors paradoxically activate its C-terminal transcriptional activity through kinase-domain conformational changes, that several reported ERK5 inhibitors act through off-target bromodomain inhibition, and that many genetic-loss phenotypes likely reflect non-catalytic functions of the protein (PMID:32170057, PMID:27679845).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1995 Medium

    Establishing that ERK5/BMK1 was a genuinely distinct MAP kinase rather than an ERK1/2 paralog set the stage for asking what unique signals it transduces.

    Evidence Molecular cloning and sequence analysis of an 816-residue kinase with a TEY motif but a divergent C-terminus and loop-12

    PMID:7646528

    Open questions at the time
    • No upstream activator or substrate identified
    • Function of the unique C-terminal domain unknown
  2. 1996 Medium

    Identifying selective activation by H2O2, distinct from ERK1/2 stimuli, provided the first physiological context (oxidative/vascular stress) for ERK5 signaling.

    Evidence Kinase activity assays with multiple stimuli and calcium chelation in vascular smooth muscle cells

    PMID:8663194

    Open questions at the time
    • Upstream kinase cascade not defined
    • Downstream effectors unknown
  3. 1998 High

    Linking ERK5 to MEF2 and to EGF-driven proliferation defined its two core outputs: direct transcription-factor coactivation and cell-cycle entry.

    Evidence Y2H, GST pulldown, Co-IP, in vitro kinase and reporter assays (MEF2); dominant-negative BMK1 with cell-cycle/BrdU analysis (EGF proliferation)

    PMID:9753748 PMID:9790194

    Open questions at the time
    • Upstream activating kinases for MEK5 not yet identified
    • Mechanism of nuclear targeting unresolved
  4. 1999 High

    Defining the MEKK3-MEK5-ERK5 cascade and a second substrate (Sap1a) built the canonical three-tier module and broadened its transcriptional reach to SRE/c-Fos.

    Evidence Y2H and reciprocal Co-IP for MEKK3-MEK5; dominant-negative genetics, in vitro kinase and reporter assays for Sap1a; mechanistic dissection of shear-stress activation

    PMID:10473620 PMID:10593883 PMID:9867822

    Open questions at the time
    • Cell-type specificity of MEKK usage not yet appreciated
    • Upstream input to MEKK3 undefined
  5. 2000 High

    Mapping the C-terminal TAD, NLS, MEF2-interaction and oligomerization modules, plus an alternative MEKK2 input and an NF-κB/RSK link, established the molecular architecture underlying ERK5's dual kinase/transcriptional nature.

    Evidence Systematic domain deletion/mutagenesis with kinase, reporter and localization readouts; Y2H/Co-IP for MEKK2; reporter and focus-formation assays for NF-κB

    PMID:11046135 PMID:11073940 PMID:11118448 PMID:11139578

    Open questions at the time
    • Signals controlling nuclear translocation only partly defined
    • Direct NF-κB substrate not identified
  6. 2001 Medium

    Identifying SGK (Ser78) and Bad-adjacent survival signaling, plus RET-Y1062 and redox/c-Src inputs, connected ERK5 to growth-factor proliferation and cell-survival programs through specific phospho-substrates and additional receptor inputs.

    Evidence Y2H, Co-IP, in vitro kinase assays with site mapping (SGK); mutagenesis and kinase/reporter assays (RET); inhibitor and dominant-negative dissection (c-Src/MEF2C); negative-feedback mapping by ERK1/2

    PMID:11237712 PMID:11254654 PMID:11478941 PMID:11782488

    Open questions at the time
    • In vivo relevance of each substrate not established
    • Hierarchy among multiple receptor inputs unclear
  7. 2002 High

    Showing ERK5 phosphorylates Bad at Ser112/136 independently of Akt/PKA/RSK and protects endothelial cells from apoptosis defined a direct anti-apoptotic mechanism.

    Evidence CA-MEK5 and DN-BMK1 overexpression, caspase-3 and MTT assays, phospho-Bad immunoblot, kinase assay

    PMID:14670836

    Open questions at the time
    • Direct vs indirect Bad phosphorylation in vivo not resolved
  8. 2003 High

    Placing WNK1 upstream of MEKK2/3 and defining the dominant-negative MEK5beta splice variant clarified pathway regulation at the input and adaptor levels.

    Evidence Co-IP, in vitro kinase assay, dominant-negative and siRNA (WNK1); Co-IP and competition assays (MEK5beta)

    PMID:14583600 PMID:14681216

    Open questions at the time
    • Physiological stimuli engaging WNK1-ERK5 not defined
    • Tissue distribution of MEK5beta unknown
  9. 2004 High

    Conditional knockout established ERK5 as essential in vivo for endothelial integrity and vascular survival, acting partly through MEF2C, anchoring the pathway in cardiovascular biology.

    Evidence Mx1-Cre and endothelial-specific knockout mice with histology; in vitro knockdown and MEF2C reporter assay

    PMID:15085193

    Open questions at the time
    • Catalytic vs non-catalytic contribution to phenotype not dissected
    • Full set of essential transcriptional targets unknown
  10. 2005 Medium

    Identifying ERK5-driven HIF1alpha degradation and a direct p90 RSK interaction extended ERK5 control to angiogenic and downstream-kinase signaling.

    Evidence Reporter, immunoblot, ubiquitination and angiogenesis/migration assays (HIF1alpha); Co-IP, in vitro kinase and domain mapping (RSK)

    PMID:15879308 PMID:16626623

    Open questions at the time
    • Mechanism by which ERK5 promotes HIF1alpha ubiquitination unclear
    • RSK activation by ERK5 contradicts prior negative finding in HeLa
  11. 2008 Medium

    Roles in keratinocyte migration/Slug, macrophage proliferation with nuclear translocation, and flow-mediated JNK suppression broadened ERK5's cellular repertoire beyond endothelium.

    Evidence shRNA and wound healing (keratinocytes); siRNA, fractionation and DNA synthesis (macrophages); selective MEK5 inhibitor BIX02188 (JNK suppression)

    PMID:18322228 PMID:18358237 PMID:18716062

    Open questions at the time
    • Direct transcriptional targets in each context not defined
    • Catalytic dependence not tested with selective tools
  12. 2009 High

    Genetic dissection separated ERK1/2 (c-Fos) from ERK5 (c-Jun) outputs and revealed ERK5-controlled inhibition of endothelial migration via p130Cas, refining the non-redundant transcriptional functions of ERK5.

    Evidence ERK5-null fibroblasts, selective MEK inhibitors and conditional kinases (c-Fos/c-Jun); CA-MEK5 retroviral transfer and migration/immunofluorescence (p130Cas)

    PMID:19249353 PMID:19605361

    Open questions at the time
    • Mechanism of c-Jun control by ERK5 not fully resolved
  13. 2010 High

    Discovering CDK1-mediated mitotic phosphorylation and the PML interaction established a MEK5-independent regulatory route and a tumor-relevant substrate, with XMD8-92 validating ERK5 as an anti-cancer target.

    Evidence Co-IP, CDK1 inhibitor, phospho-site mapping and fractionation (mitotic); Co-IP, in vitro kinase, proliferation and xenograft assays (PML/XMD8-92)

    PMID:20736311 PMID:20832753

    Open questions at the time
    • XMD8-92 specificity later questioned
    • Functional consequence of mitotic phosphorylation incompletely defined
  14. 2012 Medium

    Linking ERK5-PML to p53 suppression and defining ERK5 suppression of EMT positioned the kinase as both tumor-promoting (via PML/p53) and metastasis-restraining (via E-cadherin/Snail).

    Evidence Co-IP, reporter and tumor models (PML-MDM2-p53); siRNA/overexpression with adhesion, motility and metastasis assays (EMT)

    PMID:22282661 PMID:22869143

    Open questions at the time
    • Context determining pro- vs anti-tumor role unclear
    • Direct PML phosphosites linking to p53 axis not mapped
  15. 2013 High

    Solving the kinase-domain crystal structure and defining VHL-mediated degradation provided structural and stability-control foundations for the pathway.

    Evidence X-ray crystallography of the kinase domain with a selective inhibitor; transfection, siRNA, proteasome inhibitors (VHL degradation)

    PMID:23656407 PMID:23730213

    Open questions at the time
    • No structure of the regulatory C-terminal domain
    • Prolyl-hydroxylation/VHL recognition motif on ERK5 not defined
  16. 2014 High

    ALK-PI3K-MEKK3-MEK5-ERK5 driving MYCN in neuroblastoma, KLF2-dependent migration control, and a macrophage efferocytosis/atherosclerosis role expanded ERK5 into oncology and cardiovascular disease as a therapeutic node.

    Evidence Inhibitors, siRNA, reporter and xenograft (ALK/MYCN); CA-MEK5 with KLF2/PAK1 knockdown (migration); macrophage-specific KO with efferocytosis and atherosclerosis models

    PMID:25001623 PMID:25351247 PMID:25388666

    Open questions at the time
    • Catalytic dependence of these phenotypes not tested with clean tools
    • How ERK5 selects MYCN/KLF2 programs unclear
  17. 2015 Medium

    Mapping Thr732 phosphorylation by ERK1/2 and Pak2-dependent endothelial signaling defined additional activation/localization inputs feeding ERK5 nuclear function and vascular development.

    Evidence T732A/T732E mutagenesis, fractionation, reporter and immunofluorescence (Thr732); conditional KO and epistasis (Pak2)

    PMID:25689862 PMID:26391956

    Open questions at the time
    • Relative contribution of Thr732 vs TEY phosphorylation in vivo unclear
    • Mechanism linking Pak2 to the cascade incompletely defined
  18. 2016 High

    The discovery that kinase inhibitors paradoxically activate ERK5 transcription, that prior inhibitors acted via off-target bromodomain inhibition, and that ERK1/2 loss unmasks ERK5 as a proliferation bypass forced a major reinterpretation: many ERK5 phenotypes reflect non-catalytic functions or tool artifacts.

    Evidence Drug-resistant kinase mutants with localization/reporter assays; selective inhibitor synthesis with KINOMEscan and bromodomain profiling; Erk1/2 conditional KO with organoids and CRC lines

    PMID:27187615 PMID:27679845 PMID:32170057

    Open questions at the time
    • Which catalytic substrates retain physiological relevance unresolved
    • Mechanism of paradoxical TAD activation by inhibitors not fully structural
  19. 2017 Medium

    Defining YAP-MEKK3-MEK5-ERK5 in myogenic differentiation extended the pathway into developmental/mechanotransduction biology with a physical YAP-MEKK3 interaction.

    Evidence Co-IP, PPGY-motif and MEKK3 Y181F mutagenesis, inhibitors, differentiation assays

    PMID:28356344

    Open questions at the time
    • ERK5 transcriptional targets in myogenesis not defined
    • Catalytic dependence not isolated
  20. 2018 Medium

    Showing oncogenic BRAF enhances both ERK5 expression and nuclear localization, requiring combined MEK5/BRAF inhibition, reinforced ERK5 as a co-targetable node in RAF-driven cancers.

    Evidence siRNA, inhibitors, nuclear-ERK5 immunofluorescence, colony formation and xenograft

    PMID:29483645

    Open questions at the time
    • Mechanism by which BRAF drives ERK5 nuclear localization unclear
  21. 2020 Medium

    Establishing SUMOylation at Lys6/Lys22 as required for nuclear translocation and proliferation added a defined PTM controlling ERK5's transcriptional access.

    Evidence SUMO-site mutagenesis (K6R/K22R), immunofluorescence, immunoblot, SENP2 overexpression, proliferation assays

    PMID:32209980

    Open questions at the time
    • SUMO E3 ligase for ERK5 not identified
    • Interplay with other nuclear-targeting PTMs unresolved
  22. 2022 Medium

    Defining the PIEZO1-calcium-CaMKII-MEKK3 input clarified how mechanical shear stress is transduced to ERK5-driven KLF2/4 transcription in endothelium.

    Evidence Endothelial Piezo1 KO mice, CaMKII-MEKK3 Co-IP, inhibitors, shear-stress assays, qRT-PCR

    PMID:35883633

    Open questions at the time
    • Direct CaMKII phosphosite on MEKK3 not mapped
    • Catalytic vs scaffold role of ERK5 in KLF2/4 induction unclear
  23. 2023 High

    Identifying ERK5 S496 phosphorylation as driving SASP/senescence via NRF2 SUMOylation without altering catalytic activity provided direct in vivo proof of a kinase-independent, atheroprotective-relevant ERK5 function.

    Evidence S496A CRISPR knock-in mice, RNA-seq, imaging mass cytometry, SUMOylation and metabolic-flux assays, ERK5 inhibitors

    PMID:37264926

    Open questions at the time
    • Kinase responsible for S496 phosphorylation not defined
    • Generality of non-catalytic mechanism across other phenotypes unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved which ERK5 phenotypes depend on its catalytic kinase activity versus non-catalytic/scaffold and transcriptional functions, and the structure-function basis of its regulatory C-terminal domain is undefined.
  • Catalytic vs non-catalytic contributions not systematically separated for most substrates
  • No structure of the C-terminal TAD/NLS/MEF2-interaction region
  • Physiological substrate set under selective, on-target inhibition unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016740 transferase activity 4 GO:0140110 transcription regulator activity 3 GO:0140657 ATP-dependent activity 2
Localization
GO:0005634 nucleus 5 GO:0005829 cytosol 3 GO:0005654 nucleoplasm 2
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1640170 Cell Cycle 2 R-HSA-5357801 Programmed Cell Death 2
Partners
MEF2CMEK5MEKK2MEKK3PMLRPS6KA1SGK1WNK1
Complex memberships
MEKK2/3-MEK5-ERK5 module

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 BMK1/ERK5 is a new mammalian MAP kinase of 816 amino acids with a TEY dual phosphorylation motif (like ERK1/2) but with a distinct C-terminal domain and loop-12 structure, suggesting unique signaling functions. Molecular cloning, sequence analysis Biochemical and biophysical research communications Medium 7646528
1996 BMK1/ERK5 is a redox-sensitive kinase selectively activated by H2O2 (but not by angiotensin II, phorbol ester, PDGF, or TNF-α) in a calcium-dependent manner in vascular smooth muscle cells, demonstrating activation distinct from ERK1/2. Kinase activity assays, pharmacological inhibition, calcium chelation The Journal of biological chemistry Medium 8663194
1998 ERK5/BMK1 physically interacts with MEF2 transcription factors (interaction mapped to the MADS/MEF2 domain of MEF2); ERK5 phosphorylates MEF2 in vitro and enhances MEF2 transactivation capacity when co-expressed. Yeast two-hybrid, GST pulldown, co-immunoprecipitation, in vitro kinase assay, reporter assay Nucleic acids research High 9753748
1998 EGF-mediated activation of BMK1/ERK5 occurs independently of Ras and requires MEK5; expression of dominant-negative BMK1 blocks EGF-induced cell proliferation and prevents S-phase entry, establishing BMK1 as required for EGF-induced cell proliferation. Dominant-negative expression, cell cycle analysis, BrdU incorporation Nature High 9790194
1999 ERK5 is activated by EGF and NGF downstream of receptor tyrosine kinases via a Ras-dependent pathway; ERK5 phosphorylates the Ets-domain transcription factor Sap1a (but not Elk1) in vitro and in cells, and the ERK5 pathway mediates serum-induced c-Fos expression and serum response element transcription via Sap1a. Dominant-negative expression, reporter assay, in vitro kinase assay, phosphatase inhibition The Journal of biological chemistry High 10473620
1999 MEKK3 physically interacts with MEK5 (identified by yeast two-hybrid, confirmed by co-immunoprecipitation) and, as a dominant-active form, stimulates BMK1 activity through MEK5; endogenous MEKK3 activity is required for growth factor-mediated BMK1 activation. Yeast two-hybrid, co-immunoprecipitation, dominant-active/dominant-negative expression, kinase assay The Journal of biological chemistry High 10593883
1999 Fluid shear stress potently activates BMK1/ERK5 in endothelial cells via a mechanism dependent on non-Src tyrosine kinases and intracellular calcium, but not on Src, redox state, NO, PKA, PKC, PKG, CaM kinase, PI3K, or arachidonic acid metabolism. Kinase activity assay, pharmacological inhibitors, overexpression of kinase-inactive c-Src, calcium chelation The Journal of biological chemistry Medium 9867822
2000 MEKK2 binds MEK5 (identified by yeast two-hybrid), activates BMK1/ERK5 through MEK5, and this activation is cell-type specific (MEKK3 required in Cos7/HEK293; MEKK2 required in D10 T cells); MEKK2 also interacts with the T cell adapter Lad/RIBP and co-localizes at the T cell-APC contact site. Yeast two-hybrid, co-immunoprecipitation, dominant-negative expression, kinase assay, co-localization The Journal of biological chemistry High 11073940
2000 ERK5 contains a C-terminal transcriptional activation domain (TAD) and a MEF2-interacting domain in its C-terminal half; these domains are required for coactivation of MEF2D, and the MEF2-ERK5 interaction is activation-dependent in vivo and inhibitable by the MEF2 repressor Cabin1. Yeast two-hybrid, reporter assay, domain deletion/mutagenesis, promoter activation assays Molecular and cellular biology High 11046135
2000 ERK5 and ERK2 cooperate to activate NF-κB and induce cell transformation; the MEK5-ERK5 pathway is sufficient to activate NF-κB and p90 RSK, and ERK5 is required for NF-κB activation by RafBXB. Focus formation assay, reporter assay, dominant-negative expression, co-expression The Journal of biological chemistry Medium 11118448
2001 The C-terminal domain of ERK5 (containing a nuclear localization signal) is required for MEF2C transcriptional activation via nuclear targeting but not for kinase activation; the N-terminal domain (aa 1-77) mediates cytoplasmic targeting; aa 78-139 is required for MEK5 association; aa 140-406 is necessary for oligomerization. Mouse ERK5 splice variants mERK5b and mERK5c act as dominant-negative inhibitors of ERK5a kinase activity. Domain deletion/mutagenesis, kinase assays, reporter assays, subcellular localization (microscopy), co-immunoprecipitation The Journal of biological chemistry High 11139578
2001 BMK1 physically interacts with and phosphorylates serum- and glucocorticoid-inducible kinase (SGK) at Ser78 during growth factor stimulation; this BMK1-mediated phosphorylation is necessary for SGK activation and for growth factor-induced cell proliferation. Yeast two-hybrid, co-immunoprecipitation, in vitro kinase assay, cell proliferation assay The Journal of biological chemistry High 11254654
2001 H2O2-induced BMK1 activation in PC12 cells is mediated by c-Src (blocked by herbimycin A, PP2, and kinase-inactive Src transfection), leading to enhanced MEF2C DNA-binding activity; BMK1 pathway inhibition increases H2O2-induced cell death. Kinase activity assay, pharmacological inhibitors, dominant-negative transfection, EMSA, cell viability assay The Journal of biological chemistry Medium 11782488
2001 BMK1 is activated via RET tyrosine kinase signaling through phosphotyrosine 1062; GDNF activates BMK1 through RET-Y1062, and MEN2A RET mutation constitutively activates BMK1; this activation is not blocked by PI3K or RAS/MEK1 inhibitors, suggesting a distinct pathway from canonical Ras signaling. Site-directed mutagenesis (Y1062F), kinase assay, pharmacological inhibitors, reporter assay Biochemical and biophysical research communications Medium 11237712
2001 MKK5/ERK5 pathway activation by EGF occurs after ERK1/2 activation in HeLa cells; the classical MAPK cascade exerts negative feedback control over the MKK5/ERK5 pathway; ERK5 is not a significant activator of MAPK-activated protein kinase-1/RSK in HeLa cells (negative finding). Phospho-specific antibodies, pharmacological inhibitors (U0126, PD184352) at different concentrations FEBS letters Medium 11478941
2002 BMK1 activation protects endothelial cells from apoptosis; constitutively active MEK5 activates BMK1 and inhibits caspase-3 activity and apoptosis; BMK1 phosphorylates Bad on Ser112 and Ser136 independently of Akt, PKA, or p90RSK; dominant-negative BMK1 stimulates apoptosis and reduces Bad phosphorylation. Overexpression of CA-MEK5 and DN-BMK1, MTT assay, caspase-3 assay, phospho-Bad immunoblot, kinase assay Circulation research High 14670836
2003 WNK1 activates ERK5 through MEKK2 and MEKK3; WNK1 phosphorylates both MEKK2 and MEKK3 in vitro and activates MEKK3 in cells; MEKK2/MEKK3 co-immunoprecipitate with endogenous WNK1; ERK5 activation by EGF is attenuated by WNK1 siRNA knockdown, placing WNK1 upstream of MEKK2/3 in the ERK5 pathway. Co-immunoprecipitation, in vitro kinase assay, dominant-negative expression, siRNA knockdown The Journal of biological chemistry High 14681216
2003 MEK5beta (short splice variant) inhibits EGF-induced BMK1 activation and MEK5alpha-induced MEF2 transcriptional activity; MEK5beta co-immunoprecipitates with BMK1 and competitively prevents MEK5alpha-BMK1 association, explaining its dominant-negative behavior. Co-immunoprecipitation, kinase assay, reporter assay, overexpression of splice variants The Journal of biological chemistry Medium 14583600
2004 Conditional genetic ablation of BMK1 in adult mice leads to lethality with vascular leakage, endothelial cell rounding, misalignment, and apoptosis; endothelial-specific BMK1 KO recapitulates cardiovascular defects; in vitro BMK1 removal causes endothelial death partially via deregulation of the direct substrate MEF2C. Cardiomyocyte-specific BMK1 KO mice develop normally. Conditional knockout mice (Mx1-Cre), histology, in vitro siRNA/knockdown, MEF2C reporter assay The Journal of clinical investigation High 15085193
2005 BMK1/ERK5 negatively regulates HIF1α by promoting its ubiquitination and proteasomal degradation; constitutively active MEK5 reduces HIF1α protein levels and inhibits HIF1α-driven angiogenesis and EC migration; dominant-negative BMK1 enhances HIF1α activity. Reporter assay, immunoblot, ubiquitination inhibitors, overexpression of CA-MEK5 and DN-BMK1, Matrigel angiogenesis assay, EC migration assay Circulation research Medium 15879308
2006 ERK5 binds to and phosphorylates p90 RSK in vitro, causing RSK activation; the common docking (CD) domain of ERK5 and the D domain of RSK mediate their association; the large C-terminal domain of ERK5 is not required for RSK binding or activation; activation of ERK5 weakens its binding to RSK suggesting RSK is released upon ERK5 activation. Co-immunoprecipitation, in vitro kinase assay, domain deletion analysis Archives of biochemistry and biophysics Medium 16626623
2008 ERK5 controls EGF-induced Slug expression and keratinocyte migration; Erk5 pathway inhibition blocks keratinocyte migration and alters desmosome organization; shRNA knockdown of Erk5 reduces motility and Slug induction in response to EGF. shRNA knockdown, pharmacological inhibition, wound healing assay, immunofluorescence Molecular biology of the cell Medium 18716062
2008 In endothelial cells, MEK5-BMK1 (but not MEK1-ERK1/2) signaling mediates flow-induced inhibition of TNF-α-activated JNK; selective MEK5 inhibitor BIX02188 completely reverses the flow-mediated inhibition of JNK activation. Pharmacological inhibitors (PD184352 at selective concentrations, BIX02188), kinase assay Biochemical and biophysical research communications Medium 18358237
2008 ERK5/BMK1 is required for optimal CSF-1-induced macrophage proliferation; ERK5 activation by CSF-1 is Src family kinase-dependent; following CSF-1 stimulation, active ERK5 translocates from cytosol to nucleus; ERK5 siRNA reduces c-Jun phosphorylation/expression and increases p27 expression. siRNA knockdown, kinase assay, nuclear fractionation, immunoblot, DNA synthesis assay Journal of immunology Medium 18322228
2009 Constitutive MEK5/ERK5 activation strongly inhibits endothelial cell migration, increases focal contact number and actin stress fibers, reduces p130Cas expression (a key mediator of directed migration), and decreases focal contact turnover. Retroviral gene transfer (CA-MEK5), cell migration assay, immunofluorescence, immunoblot The Journal of biological chemistry Medium 19605361
2009 ERK1/2, but not ERK5, is necessary and sufficient for c-Fos phosphorylation and transcriptional activation; c-Fos expression is normal in ERK5−/− cells; however, ERK5−/− cells are defective for c-Jun expression, which is rescued by ERK5 re-expression. Conditional kinase activation, selective MEK inhibitors, ERK5-null fibroblasts, reporter assay Cellular signalling High 19249353
2010 CDK1 co-precipitates with ERK5 in mitotic cells and its activity is required for ERK5 phosphorylation at multiple C-terminal sites during mitosis (a second MEK5-independent phosphorylation pathway); mitotic C-terminal phosphorylation controls ERK5 nuclear-cytoplasmic shuttling and transcriptional activity. Co-immunoprecipitation, CDK1 inhibitor (RO3306), phosphorylation site mapping, subcellular fractionation, reporter assay Journal of cell science Medium 20736311
2010 BMK1 interacts with PML isoform IV and phosphorylates PML, inhibiting its tumor-suppressor function and PML-dependent p21 activation; the BMK1 inhibitor XMD8-92 blocks tumor cell proliferation in vitro and inhibits tumor growth in vivo by ~95%. Co-immunoprecipitation, in vitro kinase assay, cell proliferation assay, xenograft mouse model Cancer cell High 20832753
2012 Activated BMK1 preferentially associates with PML isoform IV and disrupts PML-MDM2 interaction, suppressing p53 activation; BMK1 deactivation combined with doxorubicin synergistically enhances MDM2 nucleolar sequestration and PML-mediated p53 upregulation. Co-immunoprecipitation, immunoblot, reporter assay, in vitro and in vivo tumor models Oncogene Medium 22869143
2012 BMK1 signaling suppresses EMT: BMK1 elevation augments E-cadherin-mediated cell-cell adhesion and reduces mesenchymal markers, while BMK1 silencing promotes Snail nuclear accumulation via Akt/GSK3β signaling activated through DEPTOR-mediated mTOR inhibition. siRNA knockdown, overexpression, immunoblot, cell adhesion/motility assay, in vivo metastasis model Cancer research Medium 22282661
2013 X-ray crystal structure of ERK5 (MAPK7) kinase domain in complex with a benzo[e]pyrimido-[5,4-b]diazepine-6(11H)-one inhibitor was determined; specific residue differences in the ATP-binding site distinguish ERK5 from ERK1/2, p38, and JNKs, providing a structural basis for inhibitor selectivity. X-ray crystallography Journal of medicinal chemistry High 23656407
2013 ERK5 is degraded via the ubiquitin-proteasome system in a process mediated by the tumor suppressor VHL through a prolyl hydroxylation-dependent mechanism; ERK5 knockdown in pVHL-negative cell lines decreases proliferation and migration. Transient transfection, siRNA knockdown, immunoblot, proteasome inhibitors Neoplasia Medium 23730213
2014 ALK activates ERK5 through a PI3K-AKT-MEKK3-MEK5 pathway; ALK-induced MYCN transcription and neuroblastoma cell proliferation require ERK5; pharmacological or siRNA inhibition of ERK5 suppresses neuroblastoma cell proliferation and enhances the anti-tumor efficacy of the ALK inhibitor crizotinib. Pharmacological inhibitors, siRNA knockdown, reporter assay, xenograft models Science signaling High 25351247
2014 ERK5 activation in macrophages promotes efferocytosis; macrophage-specific ERK5-null mice show reduced efferocytosis and accelerated atherosclerotic plaque formation on a hypercholesterolemic background. Conditional macrophage-specific ERK5 knockout mice, efferocytosis assays, atherosclerosis model Circulation High 25001623
2014 ERK5 activation inhibits endothelial cell migration via a KLF2-dependent downregulation of PAK1 mRNA and protein; KLF2 (but not KLF4) knockdown prevents ERK5-mediated PAK1 repression and restores migration capacity. Constitutively active MEK5 expression, siRNA knockdown (KLF2, KLF4, PAK1), qRT-PCR, immunoblot, migration assay Cardiovascular research Medium 25388666
2015 Pak2 (but not Pak1) signals through the Bmk1/Erk5 pathway to regulate endothelial development and function; endothelial Pak2 depletion causes embryonic lethality and adult vascular permeability; these defects are mediated through the Bmk1/Erk5 pathway. Conditional knockout mice, epistasis experiments, in vitro kinase assays Molecular and cellular biology Medium 26391956
2015 Phosphorylation of ERK5 at Thr732 by ERK1/2 (downstream of oncogenic Ras or growth factors) promotes ERK5 nuclear localization and MEF2C transcriptional activity, independently of TEY motif phosphorylation; ERK5-T732A mutant remains cytosolic under basal conditions. Site-directed mutagenesis (T732A, T732E), pharmacological inhibitors, subcellular fractionation, reporter assay, immunofluorescence PloS one Medium 25689862
2016 ERK5 kinase inhibitors paradoxically activate ERK5 transcriptional activity through its C-terminal TAD domain; inhibitor binding to the kinase domain promotes conformational changes that drive nuclear translocation and gene transcription; kinase-active drug-resistant ERK5 mutants confirmed that direct inhibitor binding to the kinase domain is required for paradoxical transcriptional activation. Drug-resistant kinase mutants, nuclear localization assay, reporter assay, kinase inhibitor panel Nature communications High 32170057
2016 Selective ERK5 kinase inhibitors (lacking bromodomain activity) have no antiinflammatory or antiproliferative activity, while previously reported ERK5 inhibitors derive their efficacy from off-target bromodomain inhibition; ERK5 genetic deletion/depletion phenotypes likely arise from non-catalytic (kinase-independent) functions of ERK5. Selective inhibitor synthesis and characterization, KINOMEscan, bromodomain binding assays, cell proliferation assays Proceedings of the National Academy of Sciences of the United States of America High 27679845
2016 Loss of Erk1/2 in intestinal epithelial cells results in supraphysiological ERK5 pathway activity; targeting both ERK1/2 and ERK5 more effectively suppresses cell proliferation than targeting either alone in intestinal organoids and CRC lines, demonstrating ERK5 as a bypass route for proliferation upon ERK1/2 abrogation. Conditional Erk1/2 knockout mice, intestinal organoids, siRNA, pharmacological inhibitors Nature communications High 27187615
2017 YAP promotes myogenic differentiation via the MEK5-ERK5 pathway through a Src/c-Abl/MEKK3 cascade; YAP physically interacts with MEKK3 (via PPGY motif at aa 178-181) and ERK5 as shown by co-immunoprecipitation; MEKK3 Y181F mutation inhibits MEK5/ERK5 activation and myogenic differentiation. Co-immunoprecipitation, site-directed mutagenesis, pharmacological inhibitors, Western blot, differentiation assays FASEB journal Medium 28356344
2018 Oncogenic BRAF positively regulates ERK5 expression, phosphorylation, and nuclear localization; both ERK5 kinase and transcriptional transactivation activities are enhanced by BRAF; combined inhibition of MEK5 and BRAFV600E is required to decrease nuclear ERK5, which is critical for cell proliferation. siRNA knockdown, pharmacological inhibitors, immunofluorescence (nuclear ERK5), colony formation assay, xenograft models Oncogene Medium 29483645
2020 ERK5 SUMOylation at Lys6/Lys22 is required for nuclear translocation and cancer cell proliferation; MEK5 activation or Cdc37 overexpression induces SUMO-2 modification of ERK5; SUMO site mutation (K6R/K22R) abolishes nuclear ERK5 localization; SENP2 overexpression abolishes endogenous ERK5 nuclear localization in response to EGF. SUMO site mutagenesis, immunofluorescence, immunoblot, cell proliferation assay, SENP2 overexpression International journal of molecular sciences Medium 32209980
2022 Shear stress activates PIEZO1, causing calcium influx that activates CaMKII, which interacts with and activates MEKK3 to promote MEKK3/MEK5/ERK5 signaling and ultimately KLF2/4 transcription; endothelial-specific Piezo1 deletion reduces KLF2/4 expression in vivo. Conditional endothelial Piezo1 KO mice, co-immunoprecipitation (CaMKII-MEKK3), pharmacological inhibitors, shear stress assays, qRT-PCR Cells Medium 35883633
2023 ERK5 S496 phosphorylation mediates senescence-associated secretory phenotype (SASP) and senescence-associated stemness in macrophages by upregulating AHR; ERK5 S496 phosphorylation induces NRF2 SUMOylation at K518, inhibiting NRF2 transcriptional activity without altering ERK5 catalytic activity; S496A knock-in mice are protected from atherosclerosis. CRISPR/Cas9 knock-in mouse (S496A), RNA sequencing, imaging mass cytometry, SUMOylation assay, metabolic flux analysis, pharmacological ERK5 inhibitors Circulation research High 37264926

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Activation of the protein kinase ERK5/BMK1 by receptor tyrosine kinases. Identification and characterization of a signaling pathway to the nucleus. The Journal of biological chemistry 451 10473620
1996 Big mitogen-activated protein kinase 1 (BMK1) is a redox-sensitive kinase. The Journal of biological chemistry 384 8663194
1998 Bmk1/Erk5 is required for cell proliferation induced by epidermal growth factor. Nature 364 9790194
2006 MAPK signalling: ERK5 versus ERK1/2. EMBO reports 333 16880823
1995 Primary structure of BMK1: a new mammalian map kinase. Biochemical and biophysical research communications 298 7646528
2006 Regulation of cellular functions by the ERK5 signalling pathway. Cellular signalling 229 16376520
2001 Effects of MAP kinase cascade inhibitors on the MKK5/ERK5 pathway. FEBS letters 229 11478941
2004 Targeted deletion of BMK1/ERK5 in adult mice perturbs vascular integrity and leads to endothelial failure. The Journal of clinical investigation 228 15085193
2000 ERK5 is a novel type of mitogen-activated protein kinase containing a transcriptional activation domain. Molecular and cellular biology 228 11046135
2012 ERK5: structure, regulation and function. Cellular signalling 182 22800864
2010 Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein. Cancer cell 174 20832753
2011 MEK5/ERK5 pathway: the first fifteen years. Biochimica et biophysica acta 161 22020294
1999 MEKK3 directly regulates MEK5 activity as part of the big mitogen-activated protein kinase 1 (BMK1) signaling pathway. The Journal of biological chemistry 160 10593883
1999 Fluid shear stress stimulates big mitogen-activated protein kinase 1 (BMK1) activity in endothelial cells. Dependence on tyrosine kinases and intracellular calcium. The Journal of biological chemistry 151 9867822
2002 Hydrogen peroxide stimulates c-Src-mediated big mitogen-activated protein kinase 1 (BMK1) and the MEF2C signaling pathway in PC12 cells: potential role in cell survival following oxidative insults. The Journal of biological chemistry 149 11782488
2003 Big mitogen-activated protein kinase (BMK1)/ERK5 protects endothelial cells from apoptosis. Circulation research 139 14670836
2004 Role of the BMK1/ERK5 signaling pathway: lessons from knockout mice. Journal of molecular medicine (Berlin, Germany) 138 15517128
1998 Interaction of myocyte enhancer factor 2 (MEF2) with a mitogen-activated protein kinase, ERK5/BMK1. Nucleic acids research 138 9753748
2008 Erk5 controls Slug expression and keratinocyte activation during wound healing. Molecular biology of the cell 135 18716062
2001 Molecular cloning of mouse ERK5/BMK1 splice variants and characterization of ERK5 functional domains. The Journal of biological chemistry 134 11139578
2003 WNK1 activates ERK5 by an MEKK2/3-dependent mechanism. The Journal of biological chemistry 123 14681216
2000 MEKK2 associates with the adapter protein Lad/RIBP and regulates the MEK5-BMK1/ERK5 pathway. The Journal of biological chemistry 122 11073940
2000 ERK5 and ERK2 cooperate to regulate NF-kappaB and cell transformation. The Journal of biological chemistry 112 11118448
2001 BMK1 mediates growth factor-induced cell proliferation through direct cellular activation of serum and glucocorticoid-inducible kinase. The Journal of biological chemistry 110 11254654
2019 Impact of ERK5 on the Hallmarks of Cancer. International journal of molecular sciences 89 30901834
2002 Cell-cycle arrest by PD184352 requires inhibition of extracellular signal-regulated kinases (ERK) 1/2 but not ERK5/BMK1. The Biochemical journal 88 12069688
2017 Oncogenic signaling of MEK5-ERK5. Cancer letters 86 28153789
2016 ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation. Nature communications 79 27187615
2016 ERK5 kinase activity is dispensable for cellular immune response and proliferation. Proceedings of the National Academy of Sciences of the United States of America 78 27679845
2009 ERK5 and the regulation of endothelial cell function. Biochemical Society transactions 71 19909257
2014 The kinase ALK stimulates the kinase ERK5 to promote the expression of the oncogene MYCN in neuroblastoma. Science signaling 69 25351247
2014 ERK5 activation in macrophages promotes efferocytosis and inhibits atherosclerosis. Circulation 68 25001623
2018 Phthalates promote prostate cancer cell proliferation through activation of ERK5 and p38. Environmental toxicology and pharmacology 65 30125794
2016 The MEK5/ERK5 signalling pathway in cancer: a promising novel therapeutic target. Drug discovery today 63 27320690
2014 The mitogen-activated protein kinase ERK5 regulates the development and growth of hepatocellular carcinoma. Gut 63 25183205
2012 ERK5 and its role in tumour development. Biochemical Society transactions 63 22260700
2018 MiR-143-3p inhibits the proliferation, cell migration and invasion of human breast cancer cells by modulating the expression of MAPK7. Biochimie 62 29360495
2020 The MEK5-ERK5 Kinase Axis Controls Lipid Metabolism in Small-Cell Lung Cancer. Cancer research 61 31969375
2021 The MEK5/ERK5 Pathway in Health and Disease. International journal of molecular sciences 60 34299213
2018 ERK5 is activated by oncogenic BRAF and promotes melanoma growth. Oncogene 60 29483645
2015 p21-Activated Kinase 2 Regulates Endothelial Development and Function through the Bmk1/Erk5 Pathway. Molecular and cellular biology 60 26391956
2016 ERK5 and Cell Proliferation: Nuclear Localization Is What Matters. Frontiers in cell and developmental biology 56 27713878
2000 Role of BMK1 in regulation of growth factor-induced cellular responses. Immunologic research 54 10852122
2008 ERK5/BMK1 is indispensable for optimal colony-stimulating factor 1 (CSF-1)-induced proliferation in macrophages in a Src-dependent fashion. Journal of immunology (Baltimore, Md. : 1950) 53 18322228
2005 BMK1/ERK5 is a novel regulator of angiogenesis by destabilizing hypoxia inducible factor 1alpha. Circulation research 53 15879308
2004 BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions. Kidney international 53 15086914
2014 Erk5 inhibits endothelial migration via KLF2-dependent down-regulation of PAK1. Cardiovascular research 51 25388666
2006 The MAP kinase ERK5 binds to and phosphorylates p90 RSK. Archives of biochemistry and biophysics 49 16626623
2022 Mechanosensitive Channel PIEZO1 Senses Shear Force to Induce KLF2/4 Expression via CaMKII/MEKK3/ERK5 Axis in Endothelial Cells. Cells 48 35883633
2009 ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos. Cellular signalling 48 19249353
2002 Vascular smooth muscle cell proliferation requires both p38 and BMK1 MAP kinases. Archives of biochemistry and biophysics 47 12054430
2012 BMK1 kinase suppresses epithelial-mesenchymal transition through the Akt/GSK3β signaling pathway. Cancer research 45 22282661
2010 Multisite phosphorylation of Erk5 in mitosis. Journal of cell science 43 20736311
2020 Paradoxical activation of the protein kinase-transcription factor ERK5 by ERK5 kinase inhibitors. Nature communications 42 32170057
2020 Targeted Avenues for Cancer Treatment: The MEK5-ERK5 Signaling Pathway. Trends in molecular medicine 41 32277933
2001 Activation of BMK1 via tyrosine 1062 in RET by GDNF and MEN2A mutation. Biochemical and biophysical research communications 41 11237712
2019 MEK5/ERK5 activation regulates colon cancer stem-like cell properties. Cell death discovery 40 30774996
2015 MAPK7 Regulates EMT Features and Modulates the Generation of CTCs. Molecular cancer research : MCR 40 25678598
2013 Structural determinants for ERK5 (MAPK7) and leucine rich repeat kinase 2 activities of benzo[e]pyrimido-[5,4-b]diazepine-6(11H)-ones. European journal of medicinal chemistry 40 24239623
2009 The signaling pathway leading to extracellular signal-regulated kinase 5 (ERK5) activation via G-proteins and ERK5-dependent neurotrophic effects. Molecular pharmacology 40 19858097
2020 Targeting the MAPK7/MMP9 axis for metastasis in primary bone cancer. Oncogene 38 32655131
2013 MEK5/ERK5 signaling suppresses estrogen receptor expression and promotes hormone-independent tumorigenesis. PloS one 37 23950888
2018 Mitochondrial Complex I activity signals antioxidant response through ERK5. Scientific reports 36 29743487
2008 Fluid shear stress inhibits TNF-mediated JNK activation via MEK5-BMK1 in endothelial cells. Biochemical and biophysical research communications 36 18358237
2004 Activation of big MAP kinase 1 (BMK1/ERK5) inhibits cardiac injury after myocardial ischemia and reperfusion. FEBS letters 36 15147905
2018 MicroRNA-143a-3p modulates preadipocyte proliferation and differentiation by targeting MAPK7. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 35 30243086
2016 Erk5 Is a Key Regulator of Naive-Primed Transition and Embryonic Stem Cell Identity. Cell reports 35 27498864
2013 ERK5/BMK1 is a novel target of the tumor suppressor VHL: implication in clear cell renal carcinoma. Neoplasia (New York, N.Y.) 34 23730213
2012 BMK1 is involved in the regulation of p53 through disrupting the PML-MDM2 interaction. Oncogene 34 22869143
2003 Differential role of MEK5alpha and MEK5beta in BMK1/ERK5 activation. The Journal of biological chemistry 33 14583600
2021 Inhibition of ERK5 Elicits Cellular Senescence in Melanoma via the Cyclin-Dependent Kinase Inhibitor p21. Cancer research 32 34799355
2020 Beyond Kinase Activity: ERK5 Nucleo-Cytoplasmic Shuttling as a Novel Target for Anticancer Therapy. International journal of molecular sciences 32 32023850
2019 The MKKK62-MKK3-MAPK7/14 module negatively regulates seed dormancy in rice. Rice (New York, N.Y.) 32 30671680
2017 MicroRNA-143 inhibits cell growth by targeting ERK5 and MAP3K7 in breast cancer. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 32 28746466
2016 MicroRNA-24 promotes 3T3-L1 adipocyte differentiation by directly targeting the MAPK7 signaling. Biochemical and biophysical research communications 32 27103442
2015 Phosphorylation of ERK5 on Thr732 is associated with ERK5 nuclear localization and ERK5-dependent transcription. PloS one 32 25689862
2023 An ERK5-NRF2 Axis Mediates Senescence-Associated Stemness and Atherosclerosis. Circulation research 31 37264926
2019 MicroRNA-374b induces endothelial-to-mesenchymal transition and early lesion formation through the inhibition of MAPK7 signaling. The Journal of pathology 31 30565701
2019 Chronic hyperglycemia regulates microglia polarization through ERK5. Aging 31 30684443
2009 MEK5/ERK5 signaling modulates endothelial cell migration and focal contact turnover. The Journal of biological chemistry 31 19605361
2020 SUMOylation Is Required for ERK5 Nuclear Translocation and ERK5-Mediated Cancer Cell Proliferation. International journal of molecular sciences 30 32209980
2014 The role of ERK5 in endothelial cell function. Biochemical Society transactions 30 25399574
2017 YAP promotes myogenic differentiation via the MEK5-ERK5 pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 29 28356344
2005 Control of body size by SMA-5, a homolog of MAP kinase BMK1/ERK5, in C. elegans. Development (Cambridge, England) 29 15944183
2022 The ERK5/NF-κB signaling pathway targets endometrial cancer proliferation and survival. Cellular and molecular life sciences : CMLS 28 36123565
2017 Rare coding variants in MAPK7 predispose to adolescent idiopathic scoliosis. Human mutation 28 28714182
2011 Targeting the BMK1 MAP kinase pathway in cancer therapy. Clinical cancer research : an official journal of the American Association for Cancer Research 28 21385929
2007 Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration. Hypertension research : official journal of the Japanese Society of Hypertension 28 18250560
2022 Clinical Significance and Regulation of ERK5 Expression and Function in Cancer. Cancers 27 35053510
2021 Molecular Mechanisms of Epithelial to Mesenchymal Transition Regulated by ERK5 Signaling. Biomolecules 27 33572742
2020 CircRNA Circ_0001721 Promotes the Progression of Osteosarcoma Through miR-372-3p/MAPK7 Axis. Cancer management and research 27 32982424
2017 Targeting BMK1 Impairs the Drug Resistance to Combined Inhibition of BRAF and MEK1/2 in Melanoma. Scientific reports 27 28387310
2017 Role of AP-2α and MAPK7 in the regulation of autocrine TGF-β/miR-200b signals to maintain epithelial-mesenchymal transition in cholangiocarcinoma. Journal of hematology & oncology 27 29084594
2015 Identification and validation of dysregulated MAPK7 (ERK5) as a novel oncogenic target in squamous cell lung and esophageal carcinoma. BMC cancer 27 26040563
2015 MAPK7 gene controls proliferation, migration and cell invasion in osteosarcoma. Molecular carcinogenesis 27 26460937
2013 X-ray crystal structure of ERK5 (MAPK7) in complex with a specific inhibitor. Journal of medicinal chemistry 27 23656407
2009 ERK5 activation enhances mesangial cell viability and collagen matrix accumulation in rat progressive glomerulonephritis. American journal of physiology. Renal physiology 27 19846573
2016 Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation. Cell cycle (Georgetown, Tex.) 26 26959608
2022 ERK5 Signalling and Resistance to ERK1/2 Pathway Therapeutics: The Path Less Travelled? Frontiers in cell and developmental biology 25 35903549
2020 Small molecule ERK5 kinase inhibitors paradoxically activate ERK5 signalling: be careful what you wish for…. Biochemical Society transactions 25 32915196

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