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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 29 Mar 2014.

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
Vulnerability of Glioblastoma Cells to Catastrophic Vacuolization and Death Induced by a Small Molecule.
New
Impact
Ernfors et al., Stockholm, Sweden. In Cell, 18 Apr 2014
The MAP kinase MKK4, identified by a shRNA screen, represents a critical signaling node.
Effect of chemical modification on the ability of pyrrolidinium fullerene to induce apoptosis of cells transformed by JAK2 V617F mutant.
New
Kasahara et al., Tokyo, Japan. In Int Immunopharmacol, 12 Apr 2014
We previously reported that pyrrolidinium fullerene markedly induced the apoptosis of JAK2 V617F mutant-induced transformed cells through the reduction of apoptosis signal-regulating kinase 1 (ASK1), following inhibition of the c-Jun N-terminal kinase (JNK) pathway.
Retaining MKP1 expression and attenuating JNK-mediated apoptosis by RIP1 for cisplatin resistance through miR-940 inhibition.
New
Lin et al., Chengdu, China. In Oncotarget, 25 Mar 2014
In addition, activation of the JNK upstream signaling kinase, MKK4, was also potentiated in RIP1 knockdown cells.
Infection by Toxoplasma gondii specifically induces host c-Myc and the genes this pivotal transcription factor regulates.
New
Boothroyd et al., Stanford, United States. In Eukaryot Cell, 14 Mar 2014
We further demonstrate that this upregulation may be mediated through JNK kinase and is unlikely to be a non-specific host response as heat-killed Toxoplasma parasites do not induce this increase and neither do nonviable parasites inside the host cell.
Ent-Kaurane Diterpenoids from Croton Tonkinensis Induce Apoptosis in Colorectal Cancer Cells through the Phosphorylation of JNK Mediated by Reactive Oxygen Species and Dual-Specificity JNK Kinase MKK4.
New
Ito et al., Takatsuki, Japan. In Anticancer Agents Med Chem, 26 Feb 2014
The dual-specificity JNK kinase MKK4 was activated in both colorectal cancer cells treated with the active CeKD, but MKK7 was not activated.
Licochalcone A Suppresses Migration and Invasion of Human Hepatocellular Carcinoma Cells through Downregulation of MKK4/JNK via NF-κB Mediated Urokinase Plasminogen Activator Expression.
New
Hsieh et al., Taiwan. In Plos One, 22 Feb 2014
LicA was also found to inhibit the expression of phosphor-JNK and phosphor-MKK4 in SK-Hep-1 cells.
A Direct in vivo RNAi screen identifies MKK4 as a key regulator of liver regeneration.
New
Impact
Zender et al., Hannover, Germany. In Cell, May 2013
Our studies identify the dual-specific kinase MKK4 as a master regulator of liver regeneration.
Using MKK4's metastasis suppressor function to identify and dissect cancer cell-microenvironment interactions during metastatic colonization.
Review
Rinker-Schaeffer et al., Chicago, United States. In Cancer Metastasis Rev, 2012
Our research indicates that the interaction of ovarian cancer cells with the omental microenvironment can activate a stress-kinase pathway involving the mitogen-activated protein kinase kinase 4 (MKK4).
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.
Exploring the function of the JNK (c-Jun N-terminal kinase) signalling pathway in physiological and pathological processes to design novel therapeutic strategies.
Review
Tournier et al., Manchester, United Kingdom. In Biochem Soc Trans, 2012
JNK (c-Jun N-terminal kinase) is a member of the MAPK (mitogen-activated protein kinase) family that regulates a range of biological processes implicated in tumorigenesis and neurodegenerative disorders.
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.
The ATAC acetyltransferase complex coordinates MAP kinases to regulate JNK target genes.
Impact
Workman et al., Kansas City, United States. In Cell, 2010
Under conditions of osmotic stress, ATAC colocalizes with c-Jun, recruits the upstream kinases Misshapen, MKK4, and JNK, and suppresses further activation of JNK.
Correction.
Impact
Davis, In Science, 1995
Lin and M. Karin are acknowledged for informing us abut the presence of an upstream in-frame initiation codon in the sequence of human MKK4/JNKK/SEK1 before publication."
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