Mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase (MEK-1/ERK) inhibitors sensitize reduced glucocorticoid response mediated by TNFalpha in human epidermal keratinocytes (HaCaT).
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K. Oka | M. Nagashima | K. Onda | T. Hirano | S. Inoue | Y. Kawakubo
[1] O. Tliba,et al. CD38 Expression Is Insensitive to Steroid Action in Cells Treated with Tumor Necrosis Factor‐{alpha} and Interferon‐{gamma} by a Mechanism Involving the Up‐Regulation of the Glucocorticoid Receptor beta Isoform , 2006, Molecular pharmacology.
[2] J. Cidlowski,et al. CD38 Expression Is Insensitive to Steroid Action in Cells Treated with Tumor Necrosis Factor-α and Interferon-γ by a Mechanism Involving the Up-Regulation of the Glucocorticoid Receptor β Isoform , 2006, Molecular Pharmacology.
[3] K. Horie-Inoue,et al. Identification of novel steroid target genes through the combination of bioinformatics and functional analysis of hormone response elements. , 2006, Biochemical and biophysical research communications.
[4] K. Yamamoto,et al. Chromatin immunoprecipitation (ChIP) scanning identifies primary glucocorticoid receptor target genes. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[5] L. Ou,et al. Superantigen-induced corticosteroid resistance of human T cells occurs through activation of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK-ERK) pathway. , 2004, The Journal of allergy and clinical immunology.
[6] P. Rothman,et al. Enhancement of MEK/ERK signaling promotes glucocorticoid resistance in CD4+ T cells , 2004 .
[7] M. Pittelkow,et al. Pemphigus Vulgaris IgG and Methylprednisolone Exhibit Reciprocal Effects on Keratinocytes* , 2004, Journal of Biological Chemistry.
[8] G. Haegeman,et al. The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. , 2003, Endocrine reviews.
[9] A. Clark. MAP kinase phosphatase 1: a novel mediator of biological effects of glucocorticoids? , 2003, The Journal of endocrinology.
[10] C. Riccardi,et al. Glucocorticoid-Induced Leucine Zipper Inhibits the Raf-Extracellular Signal-Regulated Kinase Pathway by Binding to Raf-1 , 2002, Molecular and Cellular Biology.
[11] K. Schulze-Osthoff,et al. Critical role of nuclear factor‐κB and stress‐activated protein kinases in steroid unresponsiveness , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[12] O. Kassel,et al. Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP‐1 , 2001, The EMBO journal.
[13] J. Ashwell,et al. Inhibition of AP-1 by the Glucocorticoid-inducible Protein GILZ* , 2001, The Journal of Biological Chemistry.
[14] C. Riccardi,et al. Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor kappaB. , 2001, Blood.
[15] J. Cidlowski,et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative β isoform: A mechanism for the generation of glucocorticoid resistance , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[16] R. Herrera-Esparza,et al. TNFα and IL‐6 are mediators in the blistering process of pemphigus , 2001, International journal of dermatology.
[17] S. Lamberts,et al. Natural variants of the β isoform of the human glucocorticoid receptor do not alter sensitivity to glucocorticoids , 1999, Molecular and Cellular Endocrinology.
[18] Franco Ameglio,et al. Cytokines and bullous pemphigoid. , 1999, European cytokine network.
[19] I. Adcock,et al. Corticosteroid-resistant bronchial asthma is associated with increased c-fos expression in monocytes and T lymphocytes. , 1998, The Journal of clinical investigation.
[20] P. Barnes,et al. Anti-inflammatory actions of glucocorticoids: molecular mechanisms. , 1998, Clinical science.
[21] A. Mastroianni,et al. Cytokine pattern in blister fluid and serum of patients with bullous pemphigoid: relationships with disease intensity , 1998, The British journal of dermatology.
[22] C. Riccardi,et al. A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death. , 1997, Immunity.
[23] G. Chrousos,et al. Association of Glucocorticoid Insensitivity with Increased Expression of Glucocorticoid Receptor β , 1997, The Journal of experimental medicine.
[24] W. Pratt,et al. Steroid receptor interactions with heat shock protein and immunophilin chaperones. , 1997, Endocrine reviews.
[25] P. Stork,et al. Mitogen-activated Protein Kinase Phosphatases Inactivate Stress-activated Protein Kinase Pathways in Vivo* , 1997, The Journal of Biological Chemistry.
[26] S. Szefler,et al. A novel action of IL-13: induction of diminished monocyte glucocorticoid receptor-binding affinity. , 1996, Journal of immunology.
[27] J. Fine. Management of acquired bullous skin diseases. , 1995, The New England journal of medicine.
[28] G. Chrousos,et al. Glucocorticoid receptor beta, a potential endogenous inhibitor of glucocorticoid action in humans. , 1995, The Journal of clinical investigation.
[29] S. Szefler,et al. Combination IL-2 and IL-4 reduces glucocorticoid receptor-binding affinity and T cell response to glucocorticoids. , 1993, Journal of immunology.
[30] J. Scammell,et al. Intronic hormone response elements mediate regulation of FKBP5 by progestins and glucocorticoids , 2004, Cell stress & chaperones.
[31] Bart van der Burg,et al. Glucocorticoid-induced increase in lymphocytic FKBP51 messenger ribonucleic acid expression: a potential marker for glucocorticoid sensitivity, potency, and bioavailability. , 2003, The Journal of clinical endocrinology and metabolism.
[32] P. Amerio,et al. In Vitro and In Vivo Expression of Interleukin-1α and Tumor Necrosis Factor-α mRNA in Pemphigus Vulgaris: Interleukin-1α and Tumor Necrosis Factor-α are Involved in Acantholysis , 2000 .