MAP Kinase Kinase 4

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  Subject Areas on Research

  • A double hit to kill tumor and endothelial cells by TRAIL and antiangiogenic 3TSR. 
  • A functional variant (-1304T>G) in the MKK4 promoter contributes to a decreased risk of lung cancer by increasing the promoter activity. 
  • A peptide c-Jun N-terminal kinase (JNK) inhibitor blocks mechanical allodynia after spinal nerve ligation: respective roles of JNK activation in primary sensory neurons and spinal astrocytes for neuropathic pain development and maintenance. 
  • Activation of JNK pathway in persistent pain. 
  • Bacillus anthracis spores stimulate cytokine and chemokine innate immune responses in human alveolar macrophages through multiple mitogen-activated protein kinase pathways. 
  • Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3. 
  • Bone morphogenetic protein 4 mediates myocardial ischemic injury through JNK-dependent signaling pathway. 
  • CDK4 regulation by TNFR1 and JNK is required for NF-kappaB-mediated epidermal growth control. 
  • Deciphering the signaling networks underlying simvastatin-induced apoptosis in human cancer cells: evidence for non-canonical activation of RhoA and Rac1 GTPases. 
  • Heat-shock transcription factor (HSF)-1 pathway required for Caenorhabditis elegans immunity. 
  • Induction of ERK1/2 and histone H3 phosphorylation within the outer stripe of the outer medulla of the Eker rat by 2,3,5-tris-(glutathion-S-yl)hydroquinone. 
  • Induction of mitogenic signalling in the 1LN prostate cell line on exposure to submicromolar concentrations of cadmium+. 
  • Interleukin-1beta mediates human airway epithelial cell migration via NF-kappaB. 
  • Manipulating JNK signaling with (--)-zuonin A. 
  • Optimization of 4,6-bis-anilino-1H-pyrrolo[2,3-d]pyrimidine IGF-1R tyrosine kinase inhibitors towards JNK selectivity. 
  • Regulation of the metastasis suppressor gene MKK4 in ovarian cancer. 
  • Signal transduction. Three paths to stress relief. 
  • Spinal injection of TNF-α-activated astrocytes produces persistent pain symptom mechanical allodynia by releasing monocyte chemoattractant protein-1. 
  • The MEK pathway is required for stimulation of p21(WAF1/CIP1) by transforming growth factor-beta. 
  • The c-Jun transcription factor--bipotential mediator of neuronal death, survival and regeneration. 
  • Whole-genome analysis informs breast cancer response to aromatase inhibition. 
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  Keywords of People

  • Berchuck, Andrew, James M. Ingram Professor of Gynecologic Oncology, Obstetrics and Gynecology, Gynecologic Oncology