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Fig. 5 in 2.4.6-Trichloroanisole is a potent suppressor of olfactory signal transduction

Fig. 5. Suppression by TBA, TCP, and phenol. (A) Current suppression by 1 μM TBA (A), 1 μM TCP (B), 1 μM phenol (c), and dose-suppression relation (D). Traces: black, control; red, TBA; blue, recovery. Note that the rank order is identical to that of the human perception, TCA equivalent to TBA, which is much greater than TCP. Each plot shows the average value and SD obtained from three tested cells, except for numbers shown in parentheses. Diameter of stimulus pipette was 1 μm.

Fig. 1 in 2.4.6-Trichloroanisole is a potent suppressor of olfactory signal transduction

Fig. 1. Suppression by TCA of cAMP-induced current. (A) Experimental scheme: whole-cell recording under voltage-clamp (holding potential of −50 mV in all experiments). AC, adenylyl cyclase; Golf, G protein; R, olfactory receptor protein. TCA was included in the puffer pipette at the concentration indicated in each panel, and applied to the cell by pressure ejection (50 kPa). Tip opening diameter of stimulus pipette was 1μm. Current suppression by 10 nM (B), 100 nM (c), 1 μM (D), and 10 μM (E) TCA. Control, black; drug, red; recovery, blue. Data were obtained from different cells. (F) Relation between TCA concentration and SR. Note that the concentrations indicated are the values in the puffer pipette, and the actual concentration at the cell must be much lower than these values. Numbers in parentheses indicate cells examined. Each plot shows the average value and SD.

Fig. 4 in 2.4.6-Trichloroanisole is a potent suppressor of olfactory signal transduction

Fig. 4. Least effective concentration of TCA. (A) An example showing the effect of 10 aM TCA in puffer pipette (tip opening diameter, 3.2 μm). TCA was applied for 6 s (beginning 3 s before UV light stimulation). Duration of light stimulation was 0.5 s. Traces: black, control; red, TCA; blue, recovery. (B) Schematic diagram of U-tube system. The diameter of the tip was ∼200 μm. (c) Effect of 1 aM TCA applied with a U-tube system. TCA application was conducted for ∼30 s, and duration of light stimu- lation was 0.5 s. (D) Schematic diagram of TCA ap- plication after evaporation. In this system, filter paper (1 cm × 1 cm, blue square) soaked in a solu- tion containing 30 pM TCA was placed in a syringe, and TCA was allowed to evaporate for 15 min. The vapor was then applied at a rate of 50 mL over 5 s to a second piece of filter paper soaked in 40 μL of normal Ringer solution. (E) Effect of evaporated TCA (30 pM solution). (F) Dose-suppression relation. Plots: filled circles, TCA by U-tube application; open circles, TCA by pipette application (5 s, diameter of stimulus pipettes was 1 μm); gray circles, evapo- rated TCA by pipette application (5 s, diameter of stimulus pipettes was 1 μm); filled squares, geraniol by U-tube application. Note that geraniol application does not cause any response reduction at <10−10 M, excluding a possibility of dilution error in our protocols. Each plot shows the average value and SD.

Fig. 3 in 2.4.6-Trichloroanisole is a potent suppressor of olfactory signal transduction

Fig. 3. Time-dependence of onset and offset of TCA suppression. (A) Onset time course of TCA suppression. (Left) Preexposure time was 1 s. Light indicates UV light stimulation. (Right) Preexposure time was 3 s. Data obtained from the same cell. Traces: black, control; red, 100 nM TCA; blue, recovery. (B) The suppression was plotted against the time of preexposure. Each plot shows the average value and SD. Numbers in parentheses indicate the cells examined. (c) Offset wave forms. (D) Time course of recovery. The recoveries from the current suppression by single stimulation of 1 μM TCA were plotted against the time after the odor stimulation (n = 3). Different symbols indicate data from different cells. Pipette diameter was 1 μm.

Fig. 6 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 6. Effect of callicarpanoside B on ERK activation in AAC-19 cells. AAC-19 cells were treated with or without 100, 1000 nM callicarpanoside B for 10 min, and the cell lysate was collected for Weston blot analysis showed in the upper panel. The statistics were combined from 3 separate experiments and are presented as mean ± SEM, showed in the lower panel. Student t-test, *, P <0.05; **, P <0.01.

Fig. 7 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 7. The relative binding affinity of callicarpanoside B compared with ouabain. The 3H-ouabain binding assay was utilized to determine the relative binding affinity. After preincubation with non-radioactive ouabain or callicarpanoside B to NKA for 30 min in cultured LLC-PK1 cells, 100 nM 3H-ouabain were added and incubated another 30 min. Thus, the IC50 for binding nonradioactive ouabain or callicarpanoside B to NKA was determined by competition with 3H-ouabain. The data are combined from three experiments and are presented as mean ± SD. Non-radioactive ouabain, IC50 = 0.95 ± 0.35 μM; callicarpanoside B, IC50 = 10.55 ± 3.05 μM.

Fig. 5 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 5. Effect of callicarpanoside B on NKA-mediated kinase activation in LLC-PK1 cells. A, LLCPK1 cells were treated with 10, 100, and 250 nM callicarpanoside B for 10 min, and the cell lysate was collected for Weston blot analysis showed in the upper panel. The data are combined from 3 to 8 separate experiments and are presented as mean ± SEM, shown in the lower panel. B, LLCPK1 cells were treated with 100 nM callicarpanoside B for 2, 10, 30, and 120 min, and the cell lysate was collected for Weston blot analysis, showed in the upper panel. The data are combined from 3 to 8 separate experiments and are presented as mean ± SEM. C, LLCPK1 cells were treated with 10, 100, and 250 nM callicarpanoside B for 10 min, and the cell lysate was collected for Weston blot. Probed for p-Src and showed in the upper panel. The data are combined from indicated separate experiments and are presented as mean ± SEM, shown in the lower panel. D, LLCPK1 cells were treated with 10, 100 nM callicarpanoside B for 15 min, and the lysates were fractioned into Cytosolic (Cy) and particulate (Pa) fractions for Weston blot analysis and Pa/Cy ratios of PKCε, contents were compared. The upper panel represents Western blot. The data are combined and presented as mean ± SEM of 3 independent experiments, shown in the lower panel. Student t-test, *, P <0.05; **, P <0.01.

Fig. 4 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 4. Effect of callicarpanoside B on NKA endocytosis. A, TCN-YFP-α1 cells were treated with callicarpanoside B for 6 h. Cells were fixed with Methanol. Coverslips were mounted and imaged under a fluorescence microscope described previously (Liang et al., 2006; Tian et al., 2006). B, cell surface NKA α1 was measured by biotinylation assay as described under "Experimental". Proteins were collected after treatment with different concentrations of callicarpanoside B, ouabain as a control. Cell lysates were separated by SDS-PAGE and analyzed by Western blot for NKA α1. D, quantitative dose-response endocytosed NKA α1 was calculated from four to eight independent experiments for each dose. The values are mean ± SEM. Two-way ANOVA, **, P <0.01; ***, P <0.001.

Fig. 3 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 3. Concentration curve of callicarpanoside B (2) on NKA inhibition. The purified NKA was incubated with different concentrations of compounds for 15 min, then assayed for ouabain-sensitive ATPase activity as described under Materials and Methods. The data are combined from three to five separate experiments and are presented as mean ± SEM.

Fig. 8 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 8. Effect of callicarpanoside B on cell growth. LLCPK1 cells were subcultured in 12-well plates (50,000 cells/well) and serum-starved overnight. Before treatment, three wells of day 0 were trypsinized and counted. After callicarpanoside B treatment at the indicated dose, three wells of individual control (Con) and compound-treated cells were trypsinized and counted at 48 h.

restrictedIPD-UNDECIDEDFeb 2026View details →

ClinicalTrials.gov32/100

Investigation of Lithium on Signal Transduction, Gene Expression and Brain Myo-Inositol Levels in Manic Patients

ClinicalTrials.gov study NCT00870311. IPD Sharing: Not stated. Countries: 1. Publications: 5.

ClinicalTrials.gov32/100

Evaluating the Efficacy of Neratinib on Live Cell HER2 Signaling Transduction Analysis Positive Triple Negative Breast

ClinicalTrials.gov study NCT03812393. IPD Sharing: NO. Countries: 1. Publications: 2.

closedIPD-NOFeb 2026View details →

dryad28/100

Data from: PCB126 inhibits the activation of AMPK-CREB signal transduction required for energy sensing in liver

3,3',4,4',5-pentachlorobiphenyl (PCB126), a dioxin-like PCB, elicits toxicity through a wide array of non-carcinogenic effects, including metabolic syndrome, wasting, and non-alcoholic fatty-liver disease (NAFLD). Previously, we reported decreases in the transcription of several enzymes involved in gluconeogenesis, before the early onset of lipid accumulation. Hence, this study was aimed at understanding the impact of resultant decreases gluconeogenic enzymes on growth, weight and metabolism in the liver, upon extended exposure. Male Sprague-Dawley rats (75-100 g), fed a defined AIN-93G diet, were injected (ip) with single dose of soy oil (5 ml/kg body weight; n=14) or PCB126 (5 µmol/kg; n=15), 28 d, prior euthanasia. A subset of rats from each group were fasted for 12h (vehicle (n=6) and PCB126 (n=4)). Rats only showed significant weight loss between days 14 and 28 (P<0.05) and some mortality (P=0.0413). As in our previous studies, the expression levels of enzymes involved in gluconeogenesis (Pepck-c, G6Pase, Sds, Pc and Ldh-A) and glycogenolysis (Pygl) were strongly downregulated. The decreased expression of these enzymes in PCB126 treated rats after a 12 h fast decreased hepatic glucose production from glycogen and gluconeogenic substrates, exacerbating the hypoglycemia. Additionally, PCB126 caused hepatic steatosis and decreased the expression of the transcription factor Pparα and its targets, necessary for fatty-acid oxidation. The observed metabolic disruption across multiple branches of fasting metabolism resulted from inhibition in the activation of enzyme AMPK and transcription factor CREB signaling, necessary for "sensing" energy-deprivation and the induction of enzymes that respond to the PCB126 triggered fuel crisis in liver.

opencc-zeroDec 2017View details →

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Data from: Genomic signatures of GPCR expansions reveal functional transitions in the evolution of cephalopod signal transduction

Coleoid cephalopods show unique morphological and neural novelties, such as arms with tactile and chemosensory suckers and a large complex nervous system. The evolution of such cephalopod novelties has been attributed at a genomic level to independent gene family expansions, yet the exact association and the evolutionary timing remain unclear. In the octopus genome, one such expansion occurred in the G-protein coupled receptors (GPCRs) repertoire, a superfamily of proteins that mediate signal transduction. Here we assessed the evolutionary history of this expansion and its relationship with cephalopod novelties. Using phylogenetic analyses, two cephalopod- and two octopus-specific GPCR expansions were identified. Signatures of positive selection were analysed within the four groups, and the locations of these sequences in the Octopus bimaculoides genome were inspected. Additionally, the expression profiles of octopus GPCRs across various tissues were extracted from available transcriptomic data. Our results reveal the evolutionary history of cephalopod GPCRs. Unexpanded cephalopod GPCRs shared with other bilaterians were found to be mainly nervous tissue-specific. In contrast, duplications that are shared between octopus and the bobtail squid or specific to the octopus' lineage generated copies with divergent expression patterns devoted to tissues outside of the brain. The acquisition of novel expression domains was accompanied by gene order rearrangement either through translocation or duplication and gene loss. Lastly, expansions showed signs of positive selection and some were found to form tandem clusters with shared conserved expression profiles in cephalopod innovations such as the axial nerve cord. Altogether, our results contribute to the understanding of the molecular and evolutionary history of signal transduction and provide insights into the role of this expansion during the emergence of cephalopod novelties and/or adaptations.

opencc-zeroDec 2018View details →

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Data from: Expression of taste signal transduction molecules in the caecum of common marmosets

The extraoral presence of taste signal transduction proteins has recently been reported in rodents and humans. Here, we report for the first time the presence of these signal transduction proteins in the caecum of a non-human primate, the common marmoset. Quantitative RT-PCR data on the gene expression of taste signal transduction molecules (gustducin and TRPM5) in common marmosets suggested high expression in the caecum, which was not observed in other non-human primates. Immunohistochemical analysis confirmed the specific presence of gustducin and taste receptors in marmoset caecal cells. These results may relate to the specific feeding behaviour of marmosets, which consume plant exudates, primarily gums.

opencc-zeroDec 2012View details →

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Fig. 2. Key 1H–1H in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 2. Key 1H–1H COSY and HMBC correlations of compounds 1 and 2.

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Fig. 1 in A previously undescribed phenylethanoid glycoside from Callicarpa kwangtungensis Chun acts as an agonist of the Na/K-ATPase signal transduction pathway

Fig. 1. Chemical Structure of compounds 1–14.