INT77249
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Thus, the early life stress-induced disruption of the normal stress-hyporesponsive period during infancy is accompanied by increased GR expression. | |||||||||||||||
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However, neither the time of onset nor the mechanism(s) leading to decreased GR expression during postnatal development are known. | |||||||||||||||
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In both strains, real-time RT-PCR experiments revealed that decreased expression of GR in adolescence and adulthood is, in fact, preceded by increased GR expression during early life stress exposure. | |||||||||||||||
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These findings illustrate that the impact of early life stress on gene expression changes is modulated by the genetic background and that the persistent changes in GR and egr-1 expression that arise early during postnatal developmental are reversible by chronic fluoxetine treatment during adolescence and adulthood. | |||||||||||||||
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The beneficial effect of CpdA required expression of the GR in T cells and was achieved by down regulating LFA-1 and CD44 on peripheral Th cells and by repressing IL-17 production.
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The capacity of GR to repress NF-? | |||||||||||||||
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Microarray results indicated the inhibitory effects of corticotropin-releasing factor (CRF) receptor 1 (CRFR1) and GR antagonists (antalarmin and RU486, respectively, blocked 65% of ethanol activation, P < 0.05) on gene expression activation of the B3 subcluster (Figure 4f, g). | |||||||||||||||
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Although the expressional changes were weak, duodenal expressions of glucocorticoid receptor (GR), the vitamin D receptor (VDR), and renal expressions of the parathyroid hormone receptor (PTHR) and VDR were increased following 24 h treatment with Dex. | |||||||||||||||
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Anatomical findings regarding GR-modulated inflammatory gene expression | |||||||||||||||
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Moreover, this stress exposure paradigm caused a rise in basal plasma corticosterone levels, paralleled with an increased expression of the glucocorticoid receptor (GR) and corticotropin-releasing factor (CRF) receptor 1 [78]. | |||||||||||||||
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In addition, was observed on failure day that GR as well as ? | |||||||||||||||
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Conversely, blocking the action of endogenous anti-inflammatory molecules, such as glucocorticoid hormones in transgenic mice expressing a glucocorticoid receptor (GR) antisense RNA, sharply increases microglial activation in response to MPTP, resulting in increased DAergic neuron vulnerability [8,10,11]. | |||||||||||||||
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Conversely, blocking the action of endogenous anti-inflammatory molecules, such as glucocorticoid hormones in transgenic mice expressing a glucocorticoid receptor (GR) antisense RNA, sharply increases microglial activation in response to MPTP, resulting in increased DAergic neuron vulnerability [8,10,11]. | |||||||||||||||
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Differences in GR and ? | |||||||||||||||
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The superior mnemonic performance of the handled animals could be attributed to the increased levels of GR, since they are involved in the consolidation of learned information and their activation is a prerequisite for optimal memory [5]. | |||||||||||||||
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Our results show that vertical GR decreases response strengths at 0° by ? | |||||||||||||||
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In contrast, expression of the major exon 1(10) and another brain-specific exon 1(5)-containing GR mRNAs were unchanged. | |||||||||||||||
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Because antidepressants can increase glucocorticoid receptor (GR) expression and potentially normalize the HPA axis, this has been proposed as one mechanism of action (Barden et al 1995; Holsboer 2000; Herr et al 2003). | |||||||||||||||
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along with the induction of c-fos, c-jun, and GR gene expression in human hepatoma NPLC-KC cells (Gill et al. 1998). | |||||||||||||||
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Western blot study revealed that GR level was significantly elevated in the hippocampus but not in the frontal cortex of prenatally stressed rats, whereas concentration of FKBP51 was decreased only in the former brain structure. | |||||||||||||||
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