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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 Jan 2015.

Mitogen-activated protein kinase kinase 4

MKK4, SEK1, JNK kinase
This gene encodes a dual specificity protein kinase that belongs to the Ser/Thr protein kinase family. This kinase is a direct activator of MAP kinases in response to various environmental stresses or mitogenic stimuli. It has been shown to activate MAPK8/JNK1, MAPK9/JNK2, and MAPK14/p38, but not MAPK1/ERK2 or MAPK3/ERK3. This kinase is phosphorylated, and thus activated by MAP3K1/MEKK. The knockout studies in mice suggested the roles of this kinase in mediating survival signal in T cell development, as well as in the organogenesis of liver. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: JNK, AP-1, p38, MAPK, ERK
Papers using MKK4 antibodies
Interleukin-1 (IL-1)-induced TAK1-dependent versus MEKK3-dependent NFκB activation pathways bifurcate at IL-1-receptor associated kinase modification
Supplier
Ramji Dipak P. et al., In The International Journal of Biochemistry & Cell Biology, 2006
... The non-radioactive JNK kinase assay kit was from Cell Signalling Technology whereas small interfering RNA (siRNA) were from either Qiagen [p50 NF-κB (SI02654932); p65 ...
Papers on MKK4
MiR-127 Modulates Macrophage Polarization and Promotes Lung Inflammation and Injury by Activating the JNK Pathway.
New
Shi et al., Hangzhou, China. In J Immunol, 01 Mar 2015
Mechanistically, miR-127 demonstrated to target B cell lymphoma 6 (Bcl6) and remarkably downregulated its expression and subsequently dual specificity phosphatase 1 (Dusp1), which in turn enhanced the activation of JNK kinase and hence the development of proinflammatory macrophages.
C-Jun N-terminal kinases are required for oncolytic adenovirus-mediated autophagy.
New
Fueyo et al., Houston, United States. In Oncogene, 26 Feb 2015
Thus, genetic co-ablation of JNK1 and JNK2 genes or inhibition of JNK kinase function rendered Δ24RGD-treated cells resistant to autophagy.
Pathological Axonal Death through a MAPK Cascade that Triggers a Local Energy Deficit.
New
Impact
Tessier-Lavigne et al., New York City, United States. In Cell, 15 Feb 2015
Further, MKK4, a key component in the Sarm1-MAPK pathway, is antagonized by AKT signaling, which modulates the degenerative response by limiting activation of downstream JNK signaling.
Ubiquitin-specific protease 14 regulates c-Jun N-terminal kinase signaling at the neuromuscular junction.
New
Wilson et al., In Mol Neurodegener, 10 Feb 2015
Consistent with the direct activation of MLK3 by ubiquitination, we also observed increased activation of its downstrea targets MAP kinase kinase 4 (MKK4) and c-Jun N-terminal kinase (JNK).
The effect of ROCK on TNF-α-induced CXCL8 secretion by intestinal epithelial cell lines is mediated through MKK4 and JNK signaling.
New
McGee et al., Binghamton, United States. In Cell Immunol, 07 Feb 2015
However, inhibiting ROCK suppressed TNF-induced phosphorylation of the p54 JNK isoform and phosphorylation of the upstream MKK4 kinase.
Characterization of the Neuroprotective Potential of Derivatives of the Iron Chelating Drug Deferiprone.
New
Kontoghiorghes et al., Los Angeles, United States. In Neurochem Res, 06 Feb 2015
All of the compounds were able to both inhibit the activation of p38 MAP kinase and JNK kinase and prevent the loss of PI3 kinase activity in response to a toxic stress.
Cancer-selective targeting of the NF-κB survival pathway with GADD45β/MKK7 inhibitors.
New
Impact
Franzoso et al., Napoli, Italy. In Cancer Cell, Nov 2014
Here, we identify the interaction between the NF-κB-regulated antiapoptotic factor GADD45β and the JNK kinase MKK7 as a therapeutic target in MM.
Vulnerability of glioblastoma cells to catastrophic vacuolization and death induced by a small molecule.
New
Impact
Ernfors et al., Stockholm, Sweden. In Cell, May 2014
The MAP kinase MKK4, identified by a shRNA screen, represents a critical signaling node.
Heat shock proteins in the brain: role of Hsp70, Hsp 27, and HO-1 (Hsp32) and their therapeutic potential.
Review
Liu et al., Sacramento, United States. In Transl Stroke Res, 2013
In the brain, protein kinase D phosphorylates Hsp27 following ischemia which then binds apoptosis signal-regulating kinase 1 to prevent MKK4/7, c-Jun NH(2)-terminal kinase, and Jun-induced apoptosis, and decrease infarct volumes following focal cerebral ischemia.
A Direct in vivo RNAi screen identifies MKK4 as a key regulator of liver regeneration.
Impact
Zender et al., Hannover, Germany. In Cell, 2013
Our studies identify the dual-specific kinase MKK4 as a master regulator of liver regeneration.
[Arsenic trioxide: impact on the growth and differentiation of cancer cells and possible use in cancer therapy].
Review
Mielicki et al., In Postepy Hig Med Dosw (online), 2012
It also acts on the activity of JNK kinase, glutathione, caspases, NF-ĸB nuclear factor or pro- and antiapoptotic proteins.
Metastasis suppressors in human benign prostate, intraepithelial neoplasia, and invasive cancer: their prospects as therapeutic agents.
Review
Sang et al., Tallahassee, United States. In Med Res Rev, 2012
CD44s is decreased in both PIN and cancer; Drg-1, E-cadherin, KAI-1, RKIP, and SSeCKS show similar expression between benign epithelia and PIN, but are downregulated in invasive cancer; whereas, maspin, MKK4, Nm23 and PTEN are upregulated in PIN and downregulated in cancer.
Delayed cell cycle progression in selenoprotein W-depleted cells is regulated by a mitogen-activated protein kinase kinase 4-p38/c-Jun NH2-terminal kinase-p53 pathway.
GeneRIF
Alkan et al., Davis, United States. In J Biol Chem, 2012
SEPW1 silencing increases MKK4, which activates p38gamma, p38delta, and JNK2 to phosphorylate p53 on Ser-33 and cause a transient G(1) arrest.
MAPK7 and MAP2K4 as prognostic markers in osteosarcoma.
GeneRIF
Toledo et al., São Paulo, Brazil. In Hum Pathol, 2012
Overexpression of MAP2K4 in osteosarcoma was correlated with poor treatment response, disease progression and poor overall survival.
The association between -1304T>G polymorphism in the promoter of mitogen-activated protein kinase kinase 4 gene and the risk of cervical cancer in Chinese population.
GeneRIF
Li et al., Suzhou, China. In Dna Cell Biol, 2012
the functional -1304G variant in the MKK4 promoter contributes to a decreased risk of cervical cancer
Role of ion transport in control of apoptotic cell death.
Review
Hoffmann et al., Tübingen, Germany. In Compr Physiol, 2012
Signaling involved in the modification of cell-volume regulatory ion transport during apoptosis include mitogen-activated kinases p38, JNK, ERK1/2, MEKK1, MKK4, the small G proteins Cdc42, and/or Rac and the transcription factor p53. Osmosensing involves integrin receptors, focal adhesion kinases, and tyrosine kinase receptors.
Biological and prognostic relevance of mitogen-activated protein kinases in pancreatic adenocarcinoma.
GeneRIF
Couvelard et al., Bobigny, France. In Pancreas, 2012
Suggest that in pancreatic ductal adenocarcinomas, the MKK4 protein was directly related to high cell proliferation.
Brassinosteroid regulates stomatal development by GSK3-mediated inhibition of a MAPK pathway.
Impact
Wang et al., Stanford, United States. In Nature, 2012
Complementary in vitro and in vivo assays show that BIN2 phosphorylates YDA to inhibit YDA phosphorylation of its substrate MKK4, and that activities of downstream MAPKs are reduced in brassinosteroid-deficient mutants but increased by treatment with either brassinosteroid or GSK3-kinase inhibitor.
Distinct signaling properties of mitogen-activated protein kinase kinases 4 (MKK4) and 7 (MKK7) in embryonic stem cell (ESC) differentiation.
GeneRIF
Xia et al., Cincinnati, United States. In J Biol Chem, 2012
Distinct signaling properties of mitogen-activated protein kinase kinases 4 (MKK4) and 7 (MKK7) in embryonic stem cell (ESC) differentiation.
[Neuroprotective effect of ischemic postconditioning and remote preconditioning. Prospective of clinical use].
Review
Lishmanov et al., In Angiol Sosud Khir, 2011
It was established that foregoing effect of ischemic postconditioning depended upon an activation of PKCs, ERK, Akt kinases and a decrease in the activity of JNK kinase.
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