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Open AccessJournal ArticleDOI

New Twists in Gene Regulation by Glucocorticoid Receptor: Is DNA Binding Dispensable?

Michael Karin
- 15 May 1998 - 
- Vol. 93, Iss: 4, pp 487-490
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TLDR
As GRdim/dim mice appear relatively normal and healthy under standard laboratory conditions, the most striking outcome of these experiments is that GRE-mediated gene activation is not necessary for development and survival.
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This article is published in Cell.The article was published on 1998-05-15 and is currently open access. It has received 341 citations till now. The article focuses on the topics: Regulation of gene expression.

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Mechanisms involved in the side effects of glucocorticoids

TL;DR: This review summarizes the current knowledge of the most important GC-mediated side effects from a clinical to a molecular perspective and should be helpful in predicting the potential advantages of selective GR agonists in comparison to classical GCs.
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Immunosuppressive Drugs for Kidney Transplantation

TL;DR: This review considers the use of immunosuppressive drugs in organ transplantation, focusing on renal transplantation.
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The anti-inflammatory and immunosuppressive effects of glucocorticoids, recent developments and mechanistic insights

TL;DR: A greater understanding is required of the mechanisms by which glucocorticoids exert their anti-inflammatory and immunosuppressive actions, and recent research is shedding new light on some of these mechanisms and has produced some surprising new findings.
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In vitro generation of interleukin 10-producing regulatory CD4(+) T cells is induced by immunosuppressive drugs and inhibited by T helper type 1 (Th1)- and Th2-inducing cytokines.

TL;DR: It is shown that a combination of the immunosuppressive drugs, vitamin D3 and Dexamethasone, induced human and mouse naive CD4+ T cells to differentiate in vitro into regulatory T cells, which produced only interleukin (IL)-10, but no IL-5 and interferon (IFN)-γ, and furthermore retained strong proliferative capacity.
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The Interplay between the Glucocorticoid Receptor and Nuclear Factor-κB or Activator Protein-1: Molecular Mechanisms for Gene Repression

TL;DR: The cellular signaling pathways identified as important regulators of inflammation are the signal transduction cascades mediated by the nuclear factor-kappaB and the activator protein-1, which can both be modulated by glucocorticoids.
References
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Journal ArticleDOI

Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases.

TL;DR: In chronic inflammatory diseases, such as asthma, rheumatoid arthritis, inflammatory bowel disease, and psoriasis, several cytokines recruit activated immune and inflammatory cells to the site of lesions, thereby amplifying and perpetuating the inflammatory state.
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An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death

TL;DR: Reintroduction of RelA into RelA−/− fibroblasts resulted in enhanced survival, demonstrating that the presence ofrelA is required for protection from TNF-α.
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Immunosuppression by Glucocorticoids: Inhibition of NF-κB Activity Through Induction of IκB Synthesis

TL;DR: It is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B activation in mice and cultured cells, mediated by induction of the IκBα inhibitory protein, which traps activated NF-κB in inactive cytoplasmic complexes.
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Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-κB Activation Prevents Cell Death

TL;DR: This work investigated how TNFR1 activates different effector functions; the protein kinase JNK, transcription factor NF-kappaB, and apoptosis, finding that the three responses are mediated through separate pathways.
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Steroid hormone receptors: Many Actors in search of a plot

TL;DR: Miguel Beato,’ Peter Herrlich,t and Giinther Schlitz .
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