Serum/glucocorticoid‐inducible kinase can phosphorylate the cyclic AMP response element binding protein, CREB

David, Samuel; Kalb, Robert G.

doi:10.1016/j.febslet.2005.01.040

Cited by 41 publications

(30 citation statements)

References 36 publications

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“…Spinal cord cultures were infected with these viruses; 24 h later, lysates were prepared, and immunoblotting was performed (supplemental Similarly, the abundance of ␣-kinase murine thymoma (AKT) and its activated phospho form (a downstream reporter of PI3ЈK activity) was the same under the three conditions. Glycogen synthase kinase 3␣ (GSK3␣) is a bona fide SGK target (Sakoda et al, 2003;David and Kalb, 2005), and expressing CA-SGK in neuronal culture led to an increase in the abundance of phosphoGSK3␣, but not GSK3␣ itself. The D-N-SGK did not reduce the baseline level of activation of this kinase.…”

Section: Resultsmentioning

confidence: 99%

“…It is noteworthy that BDNF-induced primary dendrite formation in cortical neurons uses the PI3ЈK signaling pathway (Dijkhuizen and Ghosh, 2005), and PI3ЈK is an upstream activator of both AKT and SGK (Kobayashi and Cohen, 1999;Park et al, 1999;David and Kalb, 2005). Finally, because SGK is a cAMP response element-binding protein (CREB) kinase (David and Kalb, 2005) and CREB is known to participate in dendrite morphogenesis (Redmond et al, 2002), this is another potential mechanism by which SGK could evoke dendrite remodeling.…”

Section: Discussionmentioning

confidence: 99%

“…The cDNA for D-N-SGK or CA-SGK was cloned into the PRPUC amplicon vector and used to generate recombinant virus as described previously (Neve et al, 1997;David and Kalb, 2005). The titer of virus used in these studies was 3-5 ϫ 10 7 pfu/ml.…”

Section: Methodsmentioning

confidence: 99%

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Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

David¹,

Stegenga²,

Hu³

et al. 2005

J. Neurosci.

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The interaction of an animal with its environment during a critical period in early postnatal life has lifelong effects on the structure and function of sensory and motor systems. To gain insight into the molecular mechanisms of experience-dependent development, we challenged young rats to adapt to a new environment that engenders novel motor behavior. Rats born in the gravitational field (1G) of the earth subsequently were reared for 2 weeks either in the absence of gravity (microgravity) or at 1G. A comparison of gene expression using microarrays led to the identification of a panel of differentially regulated transcripts. We report here that the abundance of serum-and glucocorticoid-inducible kinase (SGK) is increased in spinal cord tissue from animals reared in microgravity in comparison with 1G-reared controls. The induction of SGK expression also can be achieved by administration of glucocorticoids to animals at 1G or neurons in vitro. Expression of constitutively active SGK in neurons leads to the elaboration of neuronal dendrites and their branching. Glucocorticoids also lead to dendrite elaboration, and this effect can be abrogated by inhibiting SGK activity. Changes in the level of expression of SGK could be part of the mechanism for experience-dependent acquisition of mature neuronal properties.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

David¹,

Stegenga²,

Hu³

et al. 2005

J. Neurosci.

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“…96 Enrichment-induced Sgk1 expression is specifically mediated through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors 97 and Sgk1 can directly phosphorylate the transcription factor cyclic AMP response element-binding protein (CREB) on serine 133. 98 Sgk1 expression level is increased by acute amphetamine 36 and lysergic acid diethylamide (LSD) treatment, 36 and it is increased in the brain and peripheral tissues following psychosocial stress. 40 The upregulation of Sgk1 strongly correlates with the occurrence of cell death.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

et al. 2006

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The significant proportion of depressed patients that are resistant to monoaminergic drug therapy and the slow onset of therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs)/serotonin/noradrenaline reuptake inhibitors (SNRIs) are two major reasons for the sustained search for new antidepressants. In an attempt to identify common underlying mechanisms for fast-and slow-acting antidepressant modalities, we have examined the transcriptional changes in seven different brain regions of the rat brain induced by three clinically effective antidepressant treatments: electro convulsive therapy (ECT), sleep deprivation (SD), and fluoxetine (FLX), the most commonly used slow-onset antidepressant. Each of these antidepressant treatments was applied with the same regimen known to have clinical efficacy: 2 days of ECT (four sessions per day), 24 h of SD, and 14 days of daily treatment of FLX, respectively. Transcriptional changes were evaluated on RNA extracted from seven different brain regions using the Affymetrix rat genome microarray 230 2.0. The gene chip data were validated using in situ hybridization or autoradiography for selected genes. The major findings of the study are:1. The transcriptional changes induced by SD, ECT and SSRI display a regionally specific distribution distinct to each treatment. 2. The fast-onset, short-lived antidepressant treatments ECT and SD evoked transcriptional changes primarily in the catecholaminergic system, whereas the slow-onset antidepressant FLX treatment evoked transcriptional changes in the serotonergic system. 3. ECT and SD affect in a similar manner the same brain regions, primarily the locus coeruleus, whereas the effects of FLX were primarily in the dorsal raphe and hypothalamus, suggesting that both different regions and pathways account for fast onset but short lasting effects as compared to slow-onset but long-lasting effects. However, the similarity between effects of ECT and SD is somewhat confounded by the fact that the two treatments appear to regulate a number of transcripts in an opposite manner. 4. Multiple transcripts (e.g. brain-derived neurotrophic factor (BDNF), serum/glucocorticoidregulated kinase (Sgk1)), whose level was reported to be affected by antidepressants or behavioral manipulations, were also found to be regulated by the treatments used in the present study. Several novel findings of transcriptional regulation upon one, two or all three treatments were made, for the latter we highlight homer, erg2, HSP27, the proto oncogene ret, sulfotransferase family 1A (Sult1a1), glycerol 3-phosphate dehydrogenase (GPD3), the orphan receptor G protein-coupled receptor 88 (GPR88) and a large number of expressed sequence tags (ESTs). 5. Transcripts encoding proteins involved in synaptic plasticity in the hippocampus were strongly affected by ECT and SD, but not by FLX.The novel transcripts, concomitantly regulated by several antidepressant treatments, may represent novel targets for fast onset, long-duration antidepressants.

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“…SGK1 is a serine and threonine protein kinase activated by the mitogen-activated protein/extracellular signal-regulated kinase signaling pathway ) and known to activate many downstream molecules, including cAMP response element-binding protein (David and Kalb, 2005). SGK1 has been implicated previously in learning and memory and synaptic plasticity (Tsai et al, 2002;Ma et al, 2006).…”

Section: Sgk1 and Plasticitymentioning

confidence: 99%

A Role for Transcriptional Repressor Methyl-CpG-Binding Protein 2 and Plasticity-Related Gene Serum- and Glucocorticoid-Inducible Kinase 1 in the Induction of Inflammatory Pain States

Géranton¹,

Morenilla‐Palao²,

Hunt³

2007

Journal of Neuroscience

108

121

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Activity-dependent changes in neurons of the rat superficial dorsal horn are crucial for the induction and maintenance of neuropathic and inflammatory pain states. To identify the molecular mechanisms underlying this sensitization of superficial dorsal horn neurons, we undertook a genome-wide microarray profiling of dorsal horn gene transcripts at various times after induction of peripheral inflammation of the rat ankle joint. At early time points, upregulation of gene expression dominated, but by 7 d, downregulation was predominant. Two to 24 h after inflammation, we identified a small number of highly upregulated transcripts previously shown to be repressed by the Methyl-CpG-binding protein 2 (MeCP2), including serum-and glucocorticoid-inducible kinase (SGK1) and FK 506 binding protein 5, genes known to be important in experience-dependent plasticity. A decrease in expression of SIN3A, a corepressor in the MeCP2 silencing complex, was also found after inflammation. Phosphorylation of MeCP2 regulates activity-dependent gene transcription, and crucially we found that MeCP2 was phosphorylated in lamina I projection neurons 1 h after induction of peripheral inflammation. Lamina I projection neurons have been shown to be essential for the development of most pain states. SGK1 protein was also localized, in part, to lamina I projection neurons, and its expression in the superficial dorsal horn increased after inflammation. Furthermore, antisense knock-down of SGK1 delayed the onset of inflammatory hyperalgesia by 24 h at least. Our results uncover an unexpected complexity in the regulation of gene expression, including the modulation of transcriptional repression, that accompanies development and maintenance of an inflammatory pain state.

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Serum/glucocorticoid‐inducible kinase can phosphorylate the cyclic AMP response element binding protein, CREB

Cited by 41 publications

References 36 publications

Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

A Role for Transcriptional Repressor Methyl-CpG-Binding Protein 2 and Plasticity-Related Gene Serum- and Glucocorticoid-Inducible Kinase 1 in the Induction of Inflammatory Pain States

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