Midori Kayahara

ORCID: 0000-0002-2967-1786
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About
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Research Areas
  • Nitric Oxide and Endothelin Effects
  • Cell death mechanisms and regulation
  • Estrogen and related hormone effects
  • Anesthesia and Neurotoxicity Research
  • Hormonal and reproductive studies
  • NF-κB Signaling Pathways
  • Cytokine Signaling Pathways and Interactions
  • Immunotherapy and Immune Responses
  • Melanoma and MAPK Pathways
  • Diet, Metabolism, and Disease
  • Heavy Metal Exposure and Toxicity
  • Mesenchymal stem cell research
  • Pluripotent Stem Cells Research
  • Protein Kinase Regulation and GTPase Signaling
  • Stress Responses and Cortisol
  • Organ Transplantation Techniques and Outcomes
  • Cellular Mechanics and Interactions
  • Cardiac Ischemia and Reperfusion
  • Adrenal Hormones and Disorders
  • Lung Cancer Research Studies
  • Electron Spin Resonance Studies
  • Sulfur Compounds in Biology
  • Trace Elements in Health
  • Neuroblastoma Research and Treatments

University of Manchester
2005-2011

Kanazawa University
2010

King's College London
1997-1998

Hammersmith Hospital
1997-1998

To elucidate the physiological significance of MEK5 in vivo, we have examined effect mek5 gene elimination mice. Heterozygous mice appear to be healthy and were fertile. However, mek5−/− embryos die at approximately embryonic day 10.5 (E10.5). The phenotype includes abnormal cardiac development as well a marked decrease proliferation an increase apoptosis heart, head, dorsal regions mutant embryos. absence does not affect cell cycle progression but sensitizes mouse fibroblasts (MEFs) ability...

10.1128/mcb.25.1.336-345.2005 article EN Molecular and Cellular Biology 2004-12-15

The signaling mechanism by which JNK affects mitochondria is critical to initiate apoptosis. Here we show that the absence of provides a partial resistance toxic effect heavy metal cadmium. Both wild type and jnk −/− fibroblasts undergoing death exhibit cytosolic cytochrome c but, unlike cells, JNK‐deficient do not display increased caspase activity DNA fragmentation. apoptotic correlates with specific defect in activation Bax. We conclude JNK‐dependent regulation Bax essential mediate...

10.1016/j.febslet.2006.01.053 article EN FEBS Letters 2006-01-26

To further understand how the mitogen-activated protein kinase (MAPK) signaling pathways regulate AP-1 activity, we have elucidated physiological role of these cascades in regulation c-jun gene expression. c-Jun is a crucial component complexes and has been shown vitro to be point integration numerous signals that can differentially affect its expression as well transcriptional activity. Our strategy was based on use (i) genetically modified fibroblasts deficient components MAPK (ii)...

10.1128/mcb.25.9.3784-3792.2005 article EN Molecular and Cellular Biology 2005-04-14

ABSTRACT We have investigated the effect of nitric oxide (NO) on apoptosis in Swiss 3T3 fibroblasts and compared it to nitrosonium cation (NO+). Both species induced apoptosis, confirmed by electron microscopy, propidium iodide staining, DNA laddering activation caspases. The kinetics triggering were different for two redox species: NO+ required only a 2 hour exposure, whereas NO 24 hours. Three sources used: aqueous solutions donors, S-nitrosoglutathione S-nitroso-N-acetylpenicillamine....

10.1242/jcs.110.18.2315 article EN Journal of Cell Science 1997-09-15

Corticosteroid-binding globulin (CBG) is the principal carrier of natural glucocorticoids in circulation, and we hypothesized that it modulates glucocorticoid bioactivity (GBA). Alterations CBG, presence noncortisol, naturally occurring use potent, synthetic glucocorticoids, all make difficult to assess adrenal activity in-vivo; these problems can be addressed by a bioassay.A bioassay was developed for serum GBA physicochemical ultrafiltration-liquid chromatography-tandem mass spectrometry...

10.1111/j.1365-2265.2011.04003.x article EN Clinical Endocrinology 2011-02-21

Glucocorticoids are potent anti-inflammatory agents, acting through the glucocorticoid receptor (GR) to regulate target gene transcription. However, GR may also exert acute effects, including activation of signaling kinases such as c-Src and protein kinase B, possibly via scaffold protein, modulator nongenomic action estrogen (MNAR). MNAR inhibited transactivation in A549 cells, but HEK293 cells there was a ligand concentration-dependent biphasic effect. Transactivation driven by low...

10.1152/ajpendo.90429.2008 article EN AJP Endocrinology and Metabolism 2008-08-06

Nitric oxide and its redox related species exhibit both neuroprotective neurotoxic effects. It has been suggested that the nitrosonium cation (NO') is towards NMDA toxicity, while free radical nitric itself [I]. However, NO' releasers such as S-nitroso-N-acetyl penicillamine (SNAP) have also shown to suppress apoptotic death of neuronal PC12 cells following nerve growth factor (NGF) withdrawal [2]. In present study we investigated in detail role two species, NO', on apoptosis. We show will...

10.1042/bst026s340 article EN Biochemical Society Transactions 1998-11-01
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