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).

[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 .