Distinct and specific functions of cGMP-dependent protein kinases

Lohmann, Suzanne M.; Vaandrager, Arie B.; Smolenski, Albert; Walter, Ulrich; Jonge, Hugo R. de

doi:10.1016/s0968-0004(97)01086-4

Cited by 363 publications

(351 citation statements)

References 43 publications

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“…Two types of PKG (I and II) are represented on the tree. PKG type I is known to play a role in food-related behaviors and plasticity (reviewed in Lohmann et al, 1997). As shown in Figure 2, all the PKG type I protein sequences cluster together and appear to be derived from PKG type II sequences.…”

Section: The Locust Foraging Gene the Locust Foraging Genementioning

confidence: 98%

The locust foraging gene

Lucas

Kornfein

Chakaborty-Chatterjee

et al. 2010

Arch Insect Biochem Physiol

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Our knowledge of how genes act on the nervous system in response to the environment to generate behavioral plasticity is limited. A number of recent advancements in this area concern food-related behaviors and a specific gene family called foraging (for), which encodes a cGMPdependent protein kinase (PKG). The desert locust (Schistocerca gregaria) is notorious for its destructive feeding and long-term migratory behavior. Locust phase polyphenism is an extreme example of environmentally induced behavioral plasticity. In response to changes in population density, locusts dramatically alter their behavior, from solitary and relatively sedentary behavior to active aggregation and swarming. Very little is known about the molecular and genetic basis of this striking behavioral phenomenon. Here we initiated studies into the locust for gene by identifying, cloning, and studying expression of the gene in the locust brain. We determined the phylogenetic relationships between the locust PKG and other known PKG proteins in insects. FOR expression was found to be confined to neurons of the anterior midline of the brain, the pars intercerebralis. Our results suggest that differences in PKG enzyme activity are correlated to well-established phase-related behavioral differences. These results lay the groundwork for functional studies of the locust for gene and its possible relations to locust phase polyphenism.

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Section: The Locust Foraging Gene the Locust Foraging Genementioning

confidence: 98%

The locust foraging gene

Lucas

Kornfein

Chakaborty-Chatterjee

et al. 2010

Arch Insect Biochem Physiol

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“…As far as mammalian neurons are concerned, studies performed on rat brain and sympathetic ganglia have highlighted the existence of different variants of the ␣ 1B subunit of N channels, each with distinct functional properties (Lin et al, 1999). Functionally distinct cGMPdependent protein kinases have also been identified in neurons (Lohmann et al, 1997;Hofmann et al, 2000). They can be either soluble or anchored at the plasma membrane and reportedly mediate a wide range of biological effects.…”

Section: Discussionmentioning

confidence: 99%

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

et al. 2002

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Although data from our laboratory and others suggest that nitric oxide (NO) exerts an overall inhibitory action on high-voltageactivated Ca 2ϩ channels, conflicting observations have been reported regarding its effects on N-type channels. We performed whole-cell and cell-attached patch-clamp recordings in IMR32 cells to clarify the functional role of NO in the modulation of N channels of human neuronal cells. During depolarizing steps to ϩ10 mV from V h ϭ Ϫ90 mV, the NO donor, sodium nitroprusside (SNP; 200 M), reduced macroscopic N currents by 34% ( p Ͻ 0.01). The magnitude of inhibition was similar at all voltages tested (range, Ϫ40 to ϩ50 mV). No significant inhibition was observed when SNP was applied together with the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (300 M), or after cell treatment with the guanylate cyclase inhibitor, 1H- channel open probability by 59% and increased both the mean shut time and the null sweep probability, but it had no significant effects on channel conductance, mean open time, or latency of first openings. These data suggest that NO inhibits N-channel gating through cGMP and PKG. The consequent decrease in Ca 2ϩ influx through these channels may affect different neuronal functions, including neurotransmitter release.

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“…Using isoform-specific primers that covered exon/intron boundaries to exclude priming from genomic DNA, we identified both cGK Iα as well as Iβ, two known splice isoforms [31] (Fig. 3A).…”

Section: Verification Of Cgk I Expression and Demonstration Of Functimentioning

confidence: 99%

“…For proliferation assays, mouse cardiac fibroblasts (passage 15-20 as well as passage [27][28][29][30][31][32][33][34][35][36][37][38][39] were seeded onto 12 well plates (Greiner, Frickenhausen, Germany) at a density of 500 cells/cm 2 . Subconfluent cells were starved in medium containing 0.1 % FCS for 2 days, then cell proliferation was stimulated for 48 h by the addition of fresh medium containing 5 % FCS in the presence or absence of 8-pCPT-cGMP (Biolog, Bremen, Germany).…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Quantitative analysis of the cardiac fibroblast transcriptome—implications for NO/cGMP signaling

et al. 2004

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SummaryCardiac fibroblasts regulate tissue repair and remodeling in the heart. To quantify transcript levels in these cells we performed a comprehensive gene expression study using serial analysis of gene expression (SAGE). Among 110,169 sequenced tags we could identify 30,507 unique transcripts. A comparison of SAGE data from cardiac fibroblasts with data derived from total mouse heart revealed a number of fibroblast-specific genes. Cardiac fibroblasts expressed a specific collection of collagens, matrix proteins and metalloproteinases, growth factors, and components of signalling pathways. The NO/cGMP signalling pathway was represented by the mRNAs for α 1 and β 1 subunits of guanylyl cyclase, cGMP-dependent protein kinase type I (cGK I) and interestingly the G-kinase anchoring protein GKAP42. The expression of cGK I was verified by RT-PCR and Western Blot. To establish a functional role for cGK I in cardiac fibroblasts we studied its effect on cell proliferation. Selective activation of cGK I with a cGMP-analog inhibited the proliferation of serum-stimulated cardiac fibroblasts which express cGK I, but not higher passage fibroblasts which contain no detectable cGK I. Currently, our data suggest that cGK I mediates the inhibitory effects of the NO/cGMP pathway on cardiac fibroblast growth.Furthermore the SAGE library of transcripts expressed in cardiac fibroblasts provides a basis for future investigations into the pathological regulatory mechanisms underlying cardiac fibrosis.

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Distinct and specific functions of cGMP-dependent protein kinases

Cited by 363 publications

References 43 publications

The locust foraging gene

The locust foraging gene

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

Quantitative analysis of the cardiac fibroblast transcriptome—implications for NO/cGMP signaling

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Distinct and specific functions of cGMP-dependent protein kinases

Cited by 363 publications

References 43 publications

The locust foraging gene

The locust foraging gene

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca2+Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

Quantitative analysis of the cardiac fibroblast transcriptome—implications for NO/cGMP signaling

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cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells