C Substrate (c + substrate)

Distribution by Scientific Domains

Kinds of C Substrate

  • kinase c substrate
  • protein kinase c substrate


  • Selected Abstracts


    Regeneration-type nerve electrode using bundled microfluidic channels

    ELECTRONICS & COMMUNICATIONS IN JAPAN, Issue 4 2009
    Takafumi Suzuki
    Abstract Neural interface devices that will allow signals from the human nervous system to control external equipment are extremely important for the next generation of prosthetic systems. A novel multichannel regeneration-type nerve electrode designed to record from and stimulate peripheral nerves has been developed to allow the control of artificial hands and to generate artificial sensations. In this study a novel flexible regeneration microelectrode based on the nerve regeneration principle was designed and fabricated using MEMS technologies. The electrode, which was fabricated on a 25-m-thick parylene C substrate, has multiple fluidic channels. Each fluidic channel was 100m wide30m high1500m long and featured multiple electrodes inside them as recording and stimulating sites. They also served as guidance channels for the regenerating axons. 2009 Wiley Periodicals, Inc. Electron Comm Jpn, 92(4): 29,34, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecj.10059 [source]


    Calcium dynamics are altered in cortical neurons lacking the calmodulin-binding protein RC3

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003
    Jacqueline J. W. Van Dalen
    Abstract RC3 is a neuronal calmodulin-binding protein and protein kinase C substrate that is thought to play an important regulatory role in synaptic transmission and neuronal plasticity. Two molecules known to regulate synaptic transmission and neuronal plasticity are Ca2+ and calmodulin, and proposed mechanisms of RC3 action involve both molecules. However, physiological evidence for a role of RC3 in neuronal Ca2+ dynamics is limited. In the current study we utilized cultured cortical neurons obtained from RC3 knockout (RC3,/,) and wildtype mice (RC3+/+) and fura-2-based microscopic Ca2+ imaging to investigate a role for RC3 in neuronal Ca2+ dynamics. Immunocytochemical characterization showed that the RC3,/, cultures lack RC3 immunoreactivity, whereas cultures prepared from wildtype mice showed RC3 immunoreactivity at all ages studied. RC3+/+ and RC3,/, cultures were indistinguishable with respect to neuron density, neuronal morphology, the formation of extensive neuritic networks and the presence of glial fibrillary acidic protein (GFAP)-positive astrocytes and ,-aminobutyric acid (GABA)ergic neurons. However, the absence of RC3 in the RC3,/, neurons was found to alter neuronal Ca2+ dynamics including baseline Ca2+ levels measured under normal physiological conditions or after blockade of synaptic transmission, spontaneous intracellular Ca2+ oscillations generated by network synaptic activity, and Ca2+ responses elicited by exogenous application of N-methyl- d -aspartate (NMDA) or class I metabotropic glutamate receptor agonists. Thus, significant changes in Ca2+ dynamics occur in cortical neurons when RC3 is absent and these changes do not involve changes in gross neuronal morphology or neuronal maturation. These data provide direct physiological evidence for a regulatory role of RC3 in neuronal Ca2+ dynamics. [source]


    Experimental evidence for the attenuating effect of SOM protection on temperature sensitivity of SOM decomposition

    GLOBAL CHANGE BIOLOGY, Issue 10 2010
    JEROEN GILLABEL
    Abstract The ability to predict C cycle responses to temperature changes depends on the accurate representation of temperature sensitivity (Q10) of soil organic matter (SOM) decomposition in C models for different C pools and soil depths. Theoretically, Q10 of SOM decomposition is determined by SOM quality and availability (referred to here as SOM protection). Here, we focus on the role of SOM protection in attenuating the intrinsic, SOM quality dependent Q10. To assess the separate effects of SOM quality and protection, we incubated topsoil and subsoil samples characterized by differences in SOM protection under optimum moisture conditions at 25 C and 35 C. Although lower SOM quality in the subsoil should lead to a higher Q10 according to kinetic theory, we observed a much lower overall temperature response in subsoil compared with the topsoil. Q10 values determined for respired SOM fractions of decreasing lability within the topsoil increased from 1.9 for the most labile to 3.8 for the least labile respired SOM, whereas corresponding Q10 values for the subsoil did not show this trend (Q10 between 1.4 and 0.9). These results indicate the existence of a limiting factor that attenuates the intrinsic effect of SOM quality on Q10 in the subsoil. A parallel incubation experiment of 13C-labeled plant material added to top- and subsoil showed that decomposition of an unprotected C substrate of equal quality responds similarly to temperature changes in top- and subsoil. This further confirms that the attenuating effect on Q10 in the subsoil originates from SOM protection rather than from microbial properties or other nutrient limitations. In conclusion, we found experimental evidence that SOM protection can attenuate the intrinsic Q10 of SOM decomposition. [source]


    Tumor necrosis factor-alpha inhibits Schwann cell proliferation by up-regulating Src-suppressed protein kinase C substrate expression

    JOURNAL OF NEUROCHEMISTRY, Issue 3 2009
    Tao Tao
    Abstract Src-suppressed protein kinase C substrate (SSeCKS) is a protein kinase C substrate protein, which plays an important role in mitogenic regulatory activity. In the early stage of nerve injury, expression of SSeCKS in the PNS increases, mainly in Schwann cells (SCs). However, the exact function of SSeCKS in the regulation of SC proliferation remains unclear. In this study, we found that tumor necrosis factor-alpha (TNF-,) induced both SSeCKS , isoform expression and SC growth arrest in a dose-dependent manner. By knocking down SSeCKS , isoform expression, TNF-,-induced growth arrest in SCs was partially rescued. Concurrently, the expression of cyclin D1 was reduced and the activity of extracellular signal-regulated kinase 1/2 was decreased. A luciferase activity assay showed that cyclin D1 expression was regulated by SSeCKS at the transcription level. In addition, the cell fragments assay and immunofluorescence revealed that TNF-, prevented the translocation of cyclin D1 into the nucleus, while knocking down SSeCKS , isoform expression prompted cyclin D1 redistribution to the nucleus. In summary, our data indicate that SSeCKS may play a critical role in TNF-,-induced SC growth arrest through inhibition of cyclin D1 expression thus preventing its nuclear translocation. [source]


    CaM kinase II and protein kinase C activations mediate enhancement of long-term potentiation by nefiracetam in the rat hippocampal CA1 region

    JOURNAL OF NEUROCHEMISTRY, Issue 3 2008
    Shigeki Moriguchi
    Abstract Nefiracetam is a pyrrolidine-related nootropic drug exhibiting various pharmacological actions such as cognitive-enhancing effect. We previously showed that nefiracetam potentiates NMDA-induced currents in cultured rat cortical neurons. To address questions whether nefiracetam affects NMDA receptor-dependent synaptic plasticity in the hippocampus, we assessed effects of nefiracetam on NMDA receptor-dependent long-term potentiation (LTP) by electrophysiology and LTP-induced phosphorylation of synaptic proteins by immunoblotting analysis. Nefiracetam treatment at 1,1000 nM increased the slope of fEPSPs in a dose-dependent manner. The enhancement was associated with increased phosphorylation of ,-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor through activation of calcium/calmodulin-dependent protein kinase II (CaMKII) without affecting synapsin I phosphorylation. In addition, nefiracetam treatment increased PKC, activity in a bell-shaped dose,response curve which peaked at 10 nM, thereby increasing phosphorylation of myristoylated alanine-rich protein kinase C substrate and NMDA receptor. Nefiracetam treatment did not affect protein kinase A activity. Consistent with the bell-shaped PKC, activation, nefiracetam treatment enhanced LTP in the rat hippocampal CA1 region with the same bell-shaped dose,response curve. Furthermore, nefiracetam-induced LTP enhancement was closely associated with CaMKII and PKC, activation with concomitant increases in phosphorylation of their endogenous substrates except for synapsin I. These results suggest that nefiracetam potentiates AMPA receptor-mediated fEPSPs through CaMKII activation and enhances NMDA receptor-dependent LTP through potentiation of the post-synaptic CaMKII and protein kinase C activities. Together with potentiation of nicotinic acetylcholine receptor function, nefiracetam-enhanced AMPA and NMDA receptor functions likely contribute to improvement of cognitive function. [source]


    Microarray Analysis of Ethanol-Treated Cortical Neurons Reveals Disruption of Genes Related to the Ubiquitin-Proteasome Pathway and Protein Synthesis

    ALCOHOLISM, Issue 12 2004
    Ramana Gutala
    Background: Chronic ethanol abuse results in deleterious behavioral responses such as tolerance, dependence, reinforcement, sensitization, and craving. The objective of this research was to identify transcripts that are differentially regulated in ethanol-treated cortical neurons compared with controls by using a pathway-focused complementary DNA microarray. Methods: Cortical neurons were isolated from postconception day 14 C57BL/6 mouse fetuses and cultured according to a standard protocol. The cortical neuronal cells were treated with 100 mM ethanol for five consecutive days with a change of media every day. A homeostatic pathway-focused microarray consisting of 638 sequence-verified genes was used to measure transcripts differentially regulated in four ethanol-treated cortical neuron samples and four control samples. Quantitative real-time reverse transcriptase-polymerase chain reaction analysis was used to verify the mRNA expression levels of genes of interest detected from the microarray experiments. Results: We identified 56 down-regulated and 10 up-regulated genes in ethanol-treated cortical neurons relative to untreated controls at a 5% false-discovery rate. The expression of many genes involved in ubiquitin-proteasome and protein synthesis was decreased by ethanol, including ubiquitin B, ubiquitin-like 3, ubiquitin-conjugating enzyme E3A, 20S proteasome ,- and ,-subunits, and members of the ribosomal proteins. Furthermore, the mRNA expression of heat shock proteins, myristoylated alanine-rich protein kinase C substrate, phosphatase and tensin homolog deleted on chromosome 10, and FK506 binding protein rapamycin-associated protein (FKBP) (mTOR) was also decreased in ethanol-treated cortical neurons. Quantitative real-time reverse transcriptase-polymerase chain reaction analysis of genes involved in the ubiquitin-proteasome cascade revealed a down-regulation of these genes, thereby corroborating our microarray results. Conclusions: Our results indicate that chronic ethanol treatment of cortical neurons resulted in decreased mRNA expression of genes involving the ubiquitin-proteasome pathway and ribosomal proteins together with mTOR expression leading to disruption of protein degradation mechanism and impairment of protein synthesis machinery. [source]


    Increasing CO2 from subambient to elevated concentrations increases grassland respiration per unit of net carbon fixation

    GLOBAL CHANGE BIOLOGY, Issue 8 2006
    H. WAYNE POLLEY
    Abstract Respiration (carbon efflux) by terrestrial ecosystems is a major component of the global carbon (C) cycle, but the response of C efflux to atmospheric CO2 enrichment remains uncertain. Respiration may respond directly to an increase in the availability of C substrates at high CO2, but also may be affected indirectly by a CO2 -mediated alteration in the amount by which respiration changes per unit of change in temperature or C uptake (sensitivity of respiration to temperature or C uptake). We measured CO2 fluxes continuously during the final 2 years of a 4-year experiment on C3/C4 grassland that was exposed to a 200,560 ,mol mol,1 CO2 gradient. Flux measurements were used to determine whether CO2 treatment affected nighttime respiration rates and the response of ecosystem respiration to seasonal changes in net C uptake and air temperature. Increasing CO2 from subambient to elevated concentrations stimulated grassland respiration at night by increasing the net amount of C fixed during daylight and by increasing either the sensitivity of C efflux to daily changes in C fixation or the respiration rate in the absence of C uptake (basal ecosystem respiration rate). These latter two changes contributed to a 30,47% increase in the ratio of nighttime respiration to daytime net C influx as CO2 increased from subamient to elevated concentrations. Daily changes in net C uptake were highly correlated with variation in temperature, meaning that the shared contribution of C uptake and temperature in explaining variance in respiration rates was large. Statistically controlling for collinearity between temperature and C uptake reduced the effect of a given change in C influx on respiration. Conversely, CO2 treatment did not affect the response of grassland respiration to seasonal variation in temperature. Elevating CO2 concentration increased grassland respiration rates by increasing both net C input and respiration per unit of C input. A better understanding of how C efflux varies with substrate supply thus may be required to accurately assess the C balance of terrestrial ecosystems. [source]


    Extracytoplasmic prosthetic group ligation to apoproteins: maturation of c -type cytochromes

    MOLECULAR MICROBIOLOGY, Issue 3 2006
    Serdar Turkarslan
    Summary In all organisms, haem is post-translationally and covalently attached to c apocytochromes to produce c holocytochromes via a process called c -type cytochromes maturation, which involves numerous components. In bacteria it was not clear which of these components catalyses the extracytoplasmic haem,apocytochrome ligation per se. In this issue of Molecular Microbiology, Feissner and colleagues report that a single polypeptide from Helicobacter pylori, corresponding to the fusion of two proteins found in other organisms, performs haem ligation to a coexpressed Bordetella pertussis apocytochrome c in an Escherichia coli mutant lacking its own cytochrome c maturation proteins. This simple experimental system pinpoints the components catalysing extracytoplasmic covalent haem ligation and raises intriguing issues about the requirements for delivery of haem and apocytochrome c substrates to produce c holocytochromes. [source]