| 1. |
- Allard, Christina, et al.
(författare)
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Rasbiologiskt språkbruk i statens rättsprocess mot sameby : DN Debatt 2015-06-11
- 2015
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Annan publikation (populärvet., debatt m.m.)abstract
- Statens hantering av forskningsresultat i rättsprocessen med Girjas sameby utgör ett hot mot Sverige som rättsstat och kunskapsnation. Åratal av svensk och internationell forskning underkänns och man använder ett språkbruk som skulle kunna vara hämtat från rasbiologins tid. Nu måste staten ta sitt ansvar och börja agera som en demokratisk rättsstat, skriver 59 forskare.
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| 2. |
- Alling, Christer, et al.
(författare)
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Adaptation of signal transduction in brain
- 1994
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Ingår i: EXS. - 1023-294X. ; 71, s. 19-28
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Tidskriftsartikel (refereegranskat)abstract
- Cell culture models were used to study the effects of long-term ethanol exposure on neuronal cells. Effects on phospholipase C and phospholipase D mediated signal transduction were investigated by assaying receptor-binding, G protein function, activities of lipases, formation of second messengers and c-fos mRNA. The signal transduction cascades displayed abnormal activities from 2 to 7 days of exposure which differed from the acute effects. Phosphatidylethanol formed by phospholipase D is an abnormal lipid that may harmfully affect nerve cell function.
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| 3. |
- Alling, Christer, et al.
(författare)
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Evaluation of ethanol effects on PLC signal transduction pathways using cell lines of neuronal origin
- 1993
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Ingår i: Alcohol and alcoholism. Supplement. - 1358-6173. ; 2, s. 295-299
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Tidskriftsartikel (refereegranskat)abstract
- Human neuroblastoma cells SH-SY5Y and neuroblastoma-glioma cells NG 108-15 have been used as models for the elucidation of the effects of ethanol on receptor-mediated phospholipase C activity, c-fos mRNA expression and protein kinase C activity. Cells were exposed to ethanol (0-200 mM) for varying periods up to seven days. Agonist stimulated events were obtained in NG 108-15 cells with bradykinin and in SH-SY5Y cells with carbachol. Chronic ethanol exposure reduced the agonist-stimulated formation of inositol 1,4,5-trisphosphate in NG 108-15 cells and in SH-SY5Y cells. 100 mM ethanol for seven days increased the membrane bound and cytosolic forms of protein kinase C activity in SH-SY5Y cells. Carbachol (1 mM) induced a maximal c-fos mRNA response after 40 minutes in SH-SY5Y cells, an effect that could be mimicked through protein kinase C stimulation by phorbol esters.
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| 4. |
- Alling, Christer, et al.
(författare)
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Muscarinic receptor-stimulated expression of c-fos in neuroblastoma cells
- 1994
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Ingår i: Alcohol and alcoholism. Supplement. - 1358-6173. ; :2, s. 103-108
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Tidskriftsartikel (refereegranskat)abstract
- The intracellular signal cascade transducing muscarinic-receptor-stimulation to gene expression was investigated in human neuroblastoma SH-SY5Y cells. Naive and ethanol-exposed SH-SU5Y cells were stimulated with carbachol (CCh) and inositol 1,4-5-trisphosphate (IP3), 1,2-diacylglycerol (DAG), and c-fos mRNA levels were analyzed using a radioreceptor assay (IP3) thin-layer chromatography (DAG) and Northern blot (c-fos mRNA). Application of the muscarinic agonist CCh induced a rapid increase in (IP3), peaking within seconds after the CCh-addition. There was also an accumulation of DAG reaching maximum after 5 min of receptor-stimulation. Stimulation with CCh also induced expression of the immediate-early gene c-fos in these cells. These events were mediated via muscarinic M1 receptors and the inhibitory effects of H7, staurosporin, and RO31-7549 on the c-fos expression indicated that it was mediated via protein kinase C. Acute exposure to 100 mM ethanol inhibited the formation of IP3 and the expression of c-fos. These effects were due to an increase in the EC50 of CCh for the events. Exposure to 100 mM ethanol for 4 days caused a potentiation of these two events. The EC50 was unaffected but the maximal response was increased. These data indicate that this signal transduction system is inhibited by acute exposure to 100 mM ethanol, an effect that is compensated for after exposure to ethanol for 4 days.
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| 5. |
- Alsterfjord, Magnus, et al.
(författare)
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Plasma membrane H+-ATPase and 14-3-3 Isoforms of Arabidopsis leaves: Evidence for isoform specificity in the 14-3-3/H+-ATPase interaction
- 2004
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Ingår i: Plant and Cell Physiology. - : Oxford University Press (OUP). - 1471-9053 .- 0032-0781. ; 45:9, s. 1202-1210
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Tidskriftsartikel (refereegranskat)abstract
- The plasma membrane H+-ATPase is activated by binding of 14-3-3 protein to the phosphorylated C terminus. Considering the large number of 14-3-3 and H+-ATPase isoforms in Arabidopsis (13 and 11 expressed genes, respectively), specificity in binding may exist between 14-3-3 and H+-ATPase isoforms. We now show that the H'-ATPase is the main target for 14-3-3 binding at the plasma membrane, and that all twelve 14-3-3 istiforms tested bind to the H+-ATPase in vitro. Using specific antibodies for nine of the 14-3-3 isoforms, we show that GF14epsilon, mu, lambda, omega, chi, phi, nu, and upsilon are present in leaves, but that isolated plasma membranes lack GF14chi, phi and upsilon. Northern blots using isoform-specific probes for all 14-3-3 and H+-ATPase isoforms showed that transcripts were present for most of the isoforms. Based on mRNA levels, GF14epsilon, mu, lambda and chi are highly expressed 14-3-3 isoforms, and AHA1, 3, and 11 highly expressed H+-ATPase isoforms in leaves. However, mass peptide fingerprinting identified AHA1 and 2 with the highest score, and their presence could be confirmed by MS/MS. It may be calculated that under 'unstressed' conditions less than one percent of total 14-3-3 is attached to the H+-ATPase. However, during a condition requiring full activation of H+ pumping, as induced here by the presence of the fungal toxin fusicoccin, several percent of total 14-3-3 may be engaged in activation of the H+-ATPase.
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| 6. |
- Bernfur, Katja, et al.
(författare)
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Relative abundance of integral plasma membrane proteins in Arabidopsis leaf and root tissue determined by metabolic labeling and mass spectrometry.
- 2013
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:8
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Tidskriftsartikel (refereegranskat)abstract
- Metabolic labeling of proteins with a stable isotope ((15)N) in intact Arabidopsis plants was used for accurate determination by mass spectrometry of differences in protein abundance between plasma membranes isolated from leaves and roots. In total, 703 proteins were identified, of which 188 were predicted to be integral membrane proteins. Major classes were transporters, receptors, proteins involved in membrane trafficking and cell wall-related proteins. Forty-one of the integral proteins, including nine of the 13 isoforms of the PIP (plasma membrane intrinsic protein) aquaporin subfamily, could be identified by peptides unique to these proteins, which made it possible to determine their relative abundance in leaf and root tissue. In addition, peptides shared between isoforms gave information on the proportions of these isoforms. A comparison between our data for protein levels and corresponding data for mRNA levels in the widely used database Genevestigator showed an agreement for only about two thirds of the proteins. By contrast, localization data available in the literature for 21 of the 41 proteins show a much better agreement with our data, in particular data based on immunostaining of proteins and GUS-staining of promoter activity. Thus, although mRNA levels may provide a useful approximation for protein levels, detection and quantification of isoform-specific peptides by proteomics should generate the most reliable data for the proteome.
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| 7. |
- Ding, W Q, et al.
(författare)
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Acute ethanol exposure attenuates expression of junD in human neuroblastoma cells
- 1998
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Ingår i: Neurochemistry International. - 0197-0186. ; 33:6, s. 525-530
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Tidskriftsartikel (refereegranskat)abstract
- This study describes the effects of acute ethanol exposure on the mRNA levels of c-jun,junB and junD in the human neuroblastoma SH-SY5Y cell line. An acute exposure to 100 mM ethanol did not influence the basal and phorbol ester-induced expression of c-jun and junB, whereas the basal mRNA level of junD was attenuated by 30%. This effect was dose- and time-dependent with maximal inhibition being detected 2 h after 100 mM ethanol treatment and the mRNA levels gradually returned towards normal afterwards. Ethanol also inhibited phorbol ester-induced expression of junD. The fact that ethanol did not influence degradation of the junD mRNA suggests that acute ethanol suppresses the transcription of the gene. These results indicate that acute ethanol exerts different effects on expression of Jun transcription factors, suggesting that as compared to c-jun and junB, the junD gene may be more sensitive to acute ethanol treatment in neuronal cells.
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| 8. |
- Ding, W Q, et al.
(författare)
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Effects of ethanol on muscarinic receptor-stimulated c-fos expression in human neuroblastoma cells
- 1997
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Ingår i: Brain Research. Molecular Brain Research. - 0169-328X. ; 46:1-2, s. 77-84
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Tidskriftsartikel (refereegranskat)abstract
- The effect of ethanol exposure on muscarinic receptor-stimulated expression of c-fos was investigated in SH-SY5Y cells. Four days of ethanol exposure enhanced carbachol-stimulated c-fos mRNA expression, analyzed with Northern blot, and Fos/AP-1 binding activity, measured with gel mobility super shift assay. Pre-incubation with muscarinic antagonists or the protein kinase C inhibitor GF109203X demonstrated that, in both control and ethanol-treated cells, carbachol-induced c-fos expression was mediated via muscarinic M1 receptors and to a large extent through protein kinase C. However, phorbol ester-induced c-fos expression was unaffected in ethanol-treated cells. Acute exposure to ethanol caused a suppression of both carbachol- and phorbol ester-stimulated c-fos expression. These results demonstrate that muscarinic receptor-stimulated gene expression is sensitive to both acute and long-term ethanol exposure.
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| 9. |
- Ding, Wei-Qun, et al.
(författare)
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Ethanol exposure increases expression of c-jun and junD in human neuroblastoma cells
- 1996
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Ingår i: NeuroReport. - 1473-558X. ; 7:13, s. 2191-2195
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate the effect of ethanol exposure on the expression of fos and jun genes. Exposure of human neuroblastoma SH-SY5Y cells to ethanol for 2-4 days caused a dose-dependent increase in c-jun and junD mRNA levels, whereas mRNAs for c-fos, fosB and junB were not detectable in control or ethanol-treated cells. Four days of ethanol exposure also enhanced the AP-1 binding activity. Experiments with actinomycin D demonstrated that ethanol did not influence the degradation of c-jun and junD mRNAs. These results demonstrate that long-term exposure to ethanol increases c-jun and junD expression. This effect may be one of the mechanisms through which ethanol influences the gene regulatory system in neuronal cells.
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| 10. |
- Ding, Wei-Qun, et al.
(författare)
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Ethanol exposure potentiates fosB and junB expression induced by muscarinic receptor stimulation in neuroblastoma SH-SY5Y cells
- 1998
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Ingår i: Alcoholism: Clinical and Experimental Research. - : Wiley. - 0145-6008 .- 1530-0277. ; 22:1, s. 225-230
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Tidskriftsartikel (refereegranskat)abstract
- Muscarinic receptor stimulation and activation of protein kinase C cause an increase in fosB and junB transcripts in human neuroblastoma SH-SY5Y cells. In this study, the effect of long-term ethanol exposure on these events was investigated. Carbachol-stimulated fosB and junB expression was elevated in ethanol-exposed cells compared with control cells. The potentiation was time- and dose-dependent on ethanol. Preincubation with muscarinic antagonists or protein kinase C inhibitor demonstrated that the carbachol-stimulated increase in fosB and junB mRNA levels was primarily mediated via M1 receptors and dependent on the activity of protein kinase C in both control and ethanol-exposed cells. Long-term ethanol exposure did not influence the expression of fosB and junB induced by activation of protein kinase C with phorbol ester. These results demonstrate that the muscarinic receptor-stimulated fosB and junB expression is sensitive to ethanol exposure in SH-SY5Y cells, suggesting that these genes participate in the regulation of neuronal function in response to chronic ethanol treatment.
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