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  • 94
    Millipore ly 364947
    Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors <t>LY364947</t> (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.
    Ly 364947, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore ly 294 002 ly
    Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors <t>LY364947</t> (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.
    Ly 294 002 Ly, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris ly 255283
    Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors <t>LY364947</t> (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.
    Ly 255283, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam ly 303511
    Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors <t>LY364947</t> (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.
    Ly 303511, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Abcam ly 294002
    TGFβ1 Regulates DNMTs and Represses Hepatogenic Differentiation of Mouse MSCs (A) Schematic illustration of signaling pathways. PCC, Pearson's correlation coefficient. (B) ELISA results for TGFβ1 expression of MSCs during HD and dHD (n = 5 independent experiments). (C) qRT-PCR of DNMTs from MSCs treated with TGFβ1 during HD (n = 6 independent experiments). Symbols indicate treatments of different TGFβ1 concentrations (+, 1 ng/mL; ++, 10 ng/mL; +++, 100 ng/mL). (D–F) qRT-PCR of DNMTs from MSCs treated with TGFβ1 and various inhibitors during HD (n = 4 independent experiments) (D). LY-364947, Alk-5 inhibitor, 400 nM; SIS3, Smad2/3 inhibitor, 10 μM; SP600125, JNK inhibitor, 30 μM; SB203580, p38 inhibitor, 30 μM; PD0325901, MEK-ERK1/2 inhibitor, 1 μM; and <t>LY294002,</t> PI3K-Akt inhibitor, 25 μM. The mRNA expression from each treatment was statistically compared with a TGFβ1-treated group. Control refers to MSC-derived dHeps after 14 days. Results from qRT-PCR (E) (n = 6 independent experiments) and ELISA (F) (n = 3 independent experiments) of TGFβ1 expression at HD 14 after DNMT knockdown. (G) DNMT-inhibitor pretreatment did not affect TGFβ1 expression (n = 3 independent experiments). Symbols indicate treatments with different 5-azacytidine concentrations (+, 0.5 μM; ++, 1 μM; +++, 2 μM). (H) Representative morphological changes of MSCs treated with TGFβ1 during HD. (I) qRT-PCR of hepatogenic-specific genes in dHeps under TGFβ1 treatment (n = 5 independent experiments). (J) Hepatic functions of dHeps under TGFβ1 treatment, as represented by albumin production (n = 7 independent experiments), glycogen storage (n = 5 independent experiments), and urea production (n = 6 independent experiments). (K) Quantification of transwell migration assay (n = 3 independent experiments) of MSCs treated with TGFβ1 during HD. All quantitative data are presented as means ± SD. Statistical analyses were performed using Student’s paired t test, with significance set at ∗ p
    Ly 294002, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris ly364947
    Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or <t>LY364947</t> (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value
    Ly364947, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Tocris ly2183240
    Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or <t>LY364947</t> (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value
    Ly2183240, supplied by Tocris, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Becton Dickinson gr1 ly 6g ly 6c
    Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or <t>LY364947</t> (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value
    Gr1 Ly 6g Ly 6c, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Tocris ly 294002
    Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or <t>LY364947</t> (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value
    Ly 294002, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Millipore inhibitor treatment ly 411575
    Notch signalling inhibition increases the number of Atoh7-positive progenitors. (A) Fish at hatching stage from a double reporter line carrying the tp1:: d2GFP reporter and the atoh7::lyntdTomato reporter were used for this experiment. (B) The fish were treated with BrdU and DMSO (control) or Notch inhibitor <t>(LY-411575)</t> for 4 days. At day 4, the fish were fixed and analysed. (C) Quantification of Atoh7-positive cells (counted as lyntdTomato-positive cells) shows an increase upon Notch signalling inhibition (** P =0.001, n =1116 cells in 5 control fish and 1507 cells in 4 inhibited fish). (D-D″) Control fish show Notch signalling activation (GFP, green) and a restricted domain of Atoh7-positive cells (lyntdTomato, magenta). (E-E″) Notch-inhibited fish do not show Notch signalling activation and the atoh7 expression domain is expanded. Error bars represent s.d. Scale bars: 20 μm.
    Inhibitor Treatment Ly 411575, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Tocris ly395756
    LY37 and selective mGluR2 agonist <t>LY395756</t> (LY39) increased both surface and total protein level of GluA1 and GluA2 subunits in the cultured prefrontal neurons. (A and B) Treatment with LY37 or LY395756 significantly increased the total protein levels of both GluA1 and GluA2 subunits ( *p
    Ly395756, supplied by Tocris, used in various techniques. Bioz Stars score: 85/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Tocris ly225910
    Contribution of CCK B receptors to mitral cell excitation. A–B. CCK B -selective agonist CCK-4 evokes excitatory and suppressive spike responses. A. Histogram of spike counts over time (10 s bins) for a cell-attached spike recording from a mitral cell (CD-1 mouse) stimulated by perfusion with CCK-4 (horizontal bar). CCK-4 evoked a transient excitatory phase ( e ), followed by spike suppression ( s ), and after removal of stimulus there was a rebound excitation. B. Mean normalized spike rate for all mitral cell responses evoked by CCK-4 in CD-1 mice ( n = 7 cells, 4 excitatory, 2 mixed excitatory-suppressive, 1 suppressive). C–D. Stimulation by 1 µM CCK-8S causes spike excitation in CCK A knockout mice. C. Histogram of spike counts over time (20 s bins) for cell-attached spike recording from a mitral cell from a CCK A knockout mouse, showing excitation ( e ) in response to CCK stimulus (horizontal bar). D. Histogram of spike counts from the same cell after washout and reapplication of 1 µM CCK-8S (horizontal bar) in the presence of a CCK B -selective antagonist (5 µM LY 225910) which blocked spike excitation. E. Upper panel : mean spike rate (baseline subtracted) for mitral cells unresponsive to CCK-8S in the presence of <t>LY225910</t> ( n = 9). Lower panel : mean normalized spike rate for excitatory spike responses evoked by CCK-8S in the presence of LY225910 ( n = 3 cells). All data from CD-1 mice. F–J. Inward current underlies spike excitation in the CCK A knockout mouse. F. Whole-cell voltage clamp recording from a mitral cell from a CCK A knockout mouse stimulated with 1 µM CCK-8S (horizontal bar), showing both slow inward current and an increase in EPSC activity, including currents underlying long lasting depolarizations (LLDs) [55] . G. Histogram of EPSC counts over time (20 s bins) for the trace in F , showing excitatory effect of CCK. H. Time course of slow inward current response to CCK for the trace in F , estimated by plotting baseline values for detected EPSCs (gray circles). Black line: smoothed curve obtained by averaging window of 8 data points. I. Whole-cell current clamp recording from same cell as in F , showing strong spike excitation caused by reapplication of 1 µM CCK-8S (horizontal bar). J. Histogram of spike counts over time (20 s bins) for the voltage trace in I , showing periods of spike frequency excitation ( e ) and suppression ( s ).
    Ly225910, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Tocris ly235959
    NMDA receptor antagonism switched the effects of experimenter-administered nicotine on brain reward systems from stimulatory to inhibitory. ( a ) Rats ( n =9) were pretreated with saline or <t>LY235959</t> (1 mg/kg), and subsequently received saline or nicotine
    Ly235959, supplied by Tocris, used in various techniques. Bioz Stars score: 85/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Tocris ly288513
    NMDA receptor antagonism switched the effects of experimenter-administered nicotine on brain reward systems from stimulatory to inhibitory. ( a ) Rats ( n =9) were pretreated with saline or <t>LY235959</t> (1 mg/kg), and subsequently received saline or nicotine
    Ly288513, supplied by Tocris, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Tocris ly320135
    The effects of ACPA and <t>LY320135</t> on β -band activity in mEC layer V. (a) Example traces from layer V showing β -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 15–29 Hz. Scale bar = 200 milliseconds × 50 μ V.
    Ly320135, supplied by Tocris, used in various techniques. Bioz Stars score: 85/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Tocris ly341495
    Effects of ZJ43 and (R,S)-2-phosphono-methylpentanedioic acid (2-PMPA) on dizocilpine (MK-801)-induced cognitive deficit in the novel object recognition test. C57BL mice were injected (INJ) with by MK-801 (0.2 mg kg −1 , intraperitoneally (i.p.)) or saline 20 min after i.p. injection with: ( a ) saline (s), ZJ43 (50, 100 or 150 mg kg −1 ) or 150 mg kg −1 ZJ43 with <t>LY341495</t> (1 mg kg −1 ); ( b ) 2-PMPA (10, 50, 100 mg kg −1 ), 100 mg kg −1 2-PMPA with LY341495 (1 mg kg −1 ), or LY341495 (1 mg kg −1 ) and 30 min later placed in a chamber with two identical objects for a 10-min acquisition session (AS) 30 min. Mice were tested with one original and one novel object in a recognition session (RS) 90 min after the AS. The recognition index for the AS was calculated as: (time exploring one of the objects/ time exploring both the objects) × 100. For the RS, the recognition index was calculated as: (time exploring the novel object/ time exploring the familiar and the novel object) × 100. ( a ) Saline-treated mice attended the novel object about twice as much as the familiar object. MK801 given before the AS blocked memory of the familiar object during the RS. ZJ43 (100 and 150 mg kg −1 ) blocked the effects of MK-801. The effect of ZJ43 (150 mg kg −1 ) on MK-801 was reversed by 1 mg kg −1 of the metabotropic glutamate receptor 2/3 antagonist LY341495. ZJ43 (100 mg kg −1 ) was not effective in blocking the MK-801 effect when given immediately after the AS. n =9–24 mice per group. ( b ) 2-PMPA dose-response on MK-801-induced cognitive deficits in the novel object recognition test. 2-PMPA (100 and 150 mg kg −1 ) blocked the effect of MK-801. LY341495 (1 mg kg −1 ) blocked the effect of 2-PMPA (100 mg kg −1 ) on MK-801. n =5–24 mice per group. Data for the saline (s-s) and saline+MK-801 (s MK) are the same as in a and b , respectively.
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    94
    Tocris ly367385
    Receptor subtype-specific effects of group I mGluR activation on locomotor-related motoneuron output. A : time course plots showing that the mGluR1 antagonist <t>LY367385</t> (50 μM) blocked DHPG (5 μM)-mediated effects on locomotor burst amplitude
    Ly367385, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 103 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors LY364947 (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.

    Journal: PLoS ONE

    Article Title: The Transcription Factors Snail and Slug Activate the Transforming Growth Factor-Beta Signaling Pathway in Breast Cancer

    doi: 10.1371/journal.pone.0026514

    Figure Lengend Snippet: Treatment with a TGF-beta inhibitor reduces the migratory response to Snail and Slug. (A) Cell migration assay using MDA-MB-231, uninfected MCF-7 cells, and MCF-7 cells infected with control, Snail or Slug adenoviruses (white bars), treated with DMSO (light grey bars) or with 10 µM final of the TGF-beta inhibitors LY364947 (dark grey bars) or SB431542 (black bars) for 2 days. The X-axis represents the total number of cells in 10 fields. The data represents the average of three independent biological replicates (* T-test p-value ≤0.05, **T-test p-value ≤0.01). (B) Addition of TGF-beta inhibitor does not affect repression of cell junction molecules CDH1, DSP and CLDN4. MCF-7 cells were untreated or treated with control or Snail adenovirus, and with DMSO vehicle or SB431542 for 2 days. RNA was isolated and RT-PCR of cDNA with real-time quantitation was performed following normalization to GAPDH, and MCF-7 Day 0. The data represents the average of three independent biological replicates.

    Article Snippet: MCF-7 cells treated with or without adenovirus and with or without inhibitors [SB431542 (Sigma, S4317) or LY364947 (Sigma, L6293)] or DMSO for 2 days, were resuspended in media without FBS and 20,000 cells placed in the upper chamber on the coated membrane.

    Techniques: Cell Migration Assay, Multiple Displacement Amplification, Infection, Isolation, Reverse Transcription Polymerase Chain Reaction, Quantitation Assay

    TGFβ1 Regulates DNMTs and Represses Hepatogenic Differentiation of Mouse MSCs (A) Schematic illustration of signaling pathways. PCC, Pearson's correlation coefficient. (B) ELISA results for TGFβ1 expression of MSCs during HD and dHD (n = 5 independent experiments). (C) qRT-PCR of DNMTs from MSCs treated with TGFβ1 during HD (n = 6 independent experiments). Symbols indicate treatments of different TGFβ1 concentrations (+, 1 ng/mL; ++, 10 ng/mL; +++, 100 ng/mL). (D–F) qRT-PCR of DNMTs from MSCs treated with TGFβ1 and various inhibitors during HD (n = 4 independent experiments) (D). LY-364947, Alk-5 inhibitor, 400 nM; SIS3, Smad2/3 inhibitor, 10 μM; SP600125, JNK inhibitor, 30 μM; SB203580, p38 inhibitor, 30 μM; PD0325901, MEK-ERK1/2 inhibitor, 1 μM; and LY294002, PI3K-Akt inhibitor, 25 μM. The mRNA expression from each treatment was statistically compared with a TGFβ1-treated group. Control refers to MSC-derived dHeps after 14 days. Results from qRT-PCR (E) (n = 6 independent experiments) and ELISA (F) (n = 3 independent experiments) of TGFβ1 expression at HD 14 after DNMT knockdown. (G) DNMT-inhibitor pretreatment did not affect TGFβ1 expression (n = 3 independent experiments). Symbols indicate treatments with different 5-azacytidine concentrations (+, 0.5 μM; ++, 1 μM; +++, 2 μM). (H) Representative morphological changes of MSCs treated with TGFβ1 during HD. (I) qRT-PCR of hepatogenic-specific genes in dHeps under TGFβ1 treatment (n = 5 independent experiments). (J) Hepatic functions of dHeps under TGFβ1 treatment, as represented by albumin production (n = 7 independent experiments), glycogen storage (n = 5 independent experiments), and urea production (n = 6 independent experiments). (K) Quantification of transwell migration assay (n = 3 independent experiments) of MSCs treated with TGFβ1 during HD. All quantitative data are presented as means ± SD. Statistical analyses were performed using Student’s paired t test, with significance set at ∗ p

    Journal: Stem Cell Reports

    Article Title: DNA Methyltransferases Modulate Hepatogenic Lineage Plasticity of Mesenchymal Stromal Cells

    doi: 10.1016/j.stemcr.2017.05.008

    Figure Lengend Snippet: TGFβ1 Regulates DNMTs and Represses Hepatogenic Differentiation of Mouse MSCs (A) Schematic illustration of signaling pathways. PCC, Pearson's correlation coefficient. (B) ELISA results for TGFβ1 expression of MSCs during HD and dHD (n = 5 independent experiments). (C) qRT-PCR of DNMTs from MSCs treated with TGFβ1 during HD (n = 6 independent experiments). Symbols indicate treatments of different TGFβ1 concentrations (+, 1 ng/mL; ++, 10 ng/mL; +++, 100 ng/mL). (D–F) qRT-PCR of DNMTs from MSCs treated with TGFβ1 and various inhibitors during HD (n = 4 independent experiments) (D). LY-364947, Alk-5 inhibitor, 400 nM; SIS3, Smad2/3 inhibitor, 10 μM; SP600125, JNK inhibitor, 30 μM; SB203580, p38 inhibitor, 30 μM; PD0325901, MEK-ERK1/2 inhibitor, 1 μM; and LY294002, PI3K-Akt inhibitor, 25 μM. The mRNA expression from each treatment was statistically compared with a TGFβ1-treated group. Control refers to MSC-derived dHeps after 14 days. Results from qRT-PCR (E) (n = 6 independent experiments) and ELISA (F) (n = 3 independent experiments) of TGFβ1 expression at HD 14 after DNMT knockdown. (G) DNMT-inhibitor pretreatment did not affect TGFβ1 expression (n = 3 independent experiments). Symbols indicate treatments with different 5-azacytidine concentrations (+, 0.5 μM; ++, 1 μM; +++, 2 μM). (H) Representative morphological changes of MSCs treated with TGFβ1 during HD. (I) qRT-PCR of hepatogenic-specific genes in dHeps under TGFβ1 treatment (n = 5 independent experiments). (J) Hepatic functions of dHeps under TGFβ1 treatment, as represented by albumin production (n = 7 independent experiments), glycogen storage (n = 5 independent experiments), and urea production (n = 6 independent experiments). (K) Quantification of transwell migration assay (n = 3 independent experiments) of MSCs treated with TGFβ1 during HD. All quantitative data are presented as means ± SD. Statistical analyses were performed using Student’s paired t test, with significance set at ∗ p

    Article Snippet: Low-glucose DMEM, IMDM, DMEM/F12, 5-azacytidine, TGFβ1, and LY-364947 were purchased from Sigma-Aldrich; SP600125, SB203580, PD325901, LY294002, and SIS3 were purchased from Abcam.

    Techniques: Periodic Counter-current Chromatography, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Derivative Assay, Transwell Migration Assay

    Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or LY364947 (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value

    Journal: PLoS ONE

    Article Title: Cyclic AMP Enhances TGF? Responses of Breast Cancer Cells by Upregulating TGF? Receptor I Expression

    doi: 10.1371/journal.pone.0054261

    Figure Lengend Snippet: Smad3 and/or ERK1/2 are involved in the TGFβ-mediated regulation of genes in MDA-MB-231 cells. (A, B) MDA-MB-231 cells were transfected with siSmad3 or control siRNA (siLuc) and incubated for three days in 2D cultures before cells were treated with TGFβ1 (T) or mock-treated (M) for 24 h, lysed and analyzed for RNA expression of Smad3, p21, Cox-2, PAI-1 and TIMP-1 by Q-RT-PCR (A) or for nuclear Smad3 protein expression by Western blot analysis (B). (C, D, E) Cells in 2D cultures (C, D, E) or 3D cultures (E) were incubated for 24 h with TGFβ1 (T) or mock-treated (M) in the presence or absence of U0126 (C) or LY364947 (D, E) and analyzed for RNA expression of genes as indicated (C, D) or for nuclear Smad3 and phospho-Smad3 expression (E). GAPDH was used as a protein loading control (E). (A, C, D) Each bar represents the mean value ± SD of 3–6 independent experiments.* p-value

    Article Snippet: To test the effect of LY364947, we chose Cox-2 and TIMP-1 genes as representatives for a Smad3- and for a ERK1/2-dependent TGFβ-responsive gene, respectively.

    Techniques: Multiple Displacement Amplification, Transfection, Incubation, RNA Expression, Reverse Transcription Polymerase Chain Reaction, Expressing, Western Blot

    Notch signalling inhibition increases the number of Atoh7-positive progenitors. (A) Fish at hatching stage from a double reporter line carrying the tp1:: d2GFP reporter and the atoh7::lyntdTomato reporter were used for this experiment. (B) The fish were treated with BrdU and DMSO (control) or Notch inhibitor (LY-411575) for 4 days. At day 4, the fish were fixed and analysed. (C) Quantification of Atoh7-positive cells (counted as lyntdTomato-positive cells) shows an increase upon Notch signalling inhibition (** P =0.001, n =1116 cells in 5 control fish and 1507 cells in 4 inhibited fish). (D-D″) Control fish show Notch signalling activation (GFP, green) and a restricted domain of Atoh7-positive cells (lyntdTomato, magenta). (E-E″) Notch-inhibited fish do not show Notch signalling activation and the atoh7 expression domain is expanded. Error bars represent s.d. Scale bars: 20 μm.

    Journal: Development (Cambridge, England)

    Article Title: Notch signalling patterns retinal composition by regulating atoh7 during post-embryonic growth

    doi: 10.1242/dev.169698

    Figure Lengend Snippet: Notch signalling inhibition increases the number of Atoh7-positive progenitors. (A) Fish at hatching stage from a double reporter line carrying the tp1:: d2GFP reporter and the atoh7::lyntdTomato reporter were used for this experiment. (B) The fish were treated with BrdU and DMSO (control) or Notch inhibitor (LY-411575) for 4 days. At day 4, the fish were fixed and analysed. (C) Quantification of Atoh7-positive cells (counted as lyntdTomato-positive cells) shows an increase upon Notch signalling inhibition (** P =0.001, n =1116 cells in 5 control fish and 1507 cells in 4 inhibited fish). (D-D″) Control fish show Notch signalling activation (GFP, green) and a restricted domain of Atoh7-positive cells (lyntdTomato, magenta). (E-E″) Notch-inhibited fish do not show Notch signalling activation and the atoh7 expression domain is expanded. Error bars represent s.d. Scale bars: 20 μm.

    Article Snippet: Inhibitor treatment LY-411575 (Sigma-Aldrich) was dissolved in DMSO to a 50 mM stock concentration.

    Techniques: Inhibition, Fluorescence In Situ Hybridization, Activation Assay, Expressing

    Notch signalling inhibition shifts cell-fate ratios within the Atoh7 lineage. (A) Wild-type fish were treated at hatch with BrdU and DMSO (control) or Notch inhibitor (LY-411575) for 4 days. At day 4, the BrdU and the DMSO or the inhibitor were washed out and the fish were grown for 14 days. At day 18, the fish were fixed and analysed. (B-B″) Control retinae display a normal morphology and the BrdU (magenta) stripe corresponding to the treatment time contains cells in the three cellular layers. The PRCs labelled with Zpr-1 (green) also display a normal morphology. (C-C″) Treated retinae display a disrupted morphology at the BrdU stripe, lacking the PRCs. (D-F) Quantification of BrdU-positive cells located in each layer in control conditions as well as in Notch-inhibited conditions reveals an increase in cells added to the INL and a decrease in photoreceptors located in the ONL (GCL: P =0.9372, n =710 cells in 3 control retinae and 1303 cells in 3 inhibited retinae; INL: ** P =0.0042, n =1104 cells in 3 control retinae and 2443 cells in 3 inhibited retinae; ONL: ** P =0.0013, n =334 cells in 3 control retinae and 169 cells in 3 inhibited retinae). Error bars represent s.d. Scale bars: 20 μm.

    Journal: Development (Cambridge, England)

    Article Title: Notch signalling patterns retinal composition by regulating atoh7 during post-embryonic growth

    doi: 10.1242/dev.169698

    Figure Lengend Snippet: Notch signalling inhibition shifts cell-fate ratios within the Atoh7 lineage. (A) Wild-type fish were treated at hatch with BrdU and DMSO (control) or Notch inhibitor (LY-411575) for 4 days. At day 4, the BrdU and the DMSO or the inhibitor were washed out and the fish were grown for 14 days. At day 18, the fish were fixed and analysed. (B-B″) Control retinae display a normal morphology and the BrdU (magenta) stripe corresponding to the treatment time contains cells in the three cellular layers. The PRCs labelled with Zpr-1 (green) also display a normal morphology. (C-C″) Treated retinae display a disrupted morphology at the BrdU stripe, lacking the PRCs. (D-F) Quantification of BrdU-positive cells located in each layer in control conditions as well as in Notch-inhibited conditions reveals an increase in cells added to the INL and a decrease in photoreceptors located in the ONL (GCL: P =0.9372, n =710 cells in 3 control retinae and 1303 cells in 3 inhibited retinae; INL: ** P =0.0042, n =1104 cells in 3 control retinae and 2443 cells in 3 inhibited retinae; ONL: ** P =0.0013, n =334 cells in 3 control retinae and 169 cells in 3 inhibited retinae). Error bars represent s.d. Scale bars: 20 μm.

    Article Snippet: Inhibitor treatment LY-411575 (Sigma-Aldrich) was dissolved in DMSO to a 50 mM stock concentration.

    Techniques: Inhibition, Fluorescence In Situ Hybridization

    LY37 and selective mGluR2 agonist LY395756 (LY39) increased both surface and total protein level of GluA1 and GluA2 subunits in the cultured prefrontal neurons. (A and B) Treatment with LY37 or LY395756 significantly increased the total protein levels of both GluA1 and GluA2 subunits ( *p

    Journal: PLoS ONE

    Article Title: Group II Metabotropic Glutamate Receptor Agonist LY379268 Regulates AMPA Receptor Trafficking in Prefrontal Cortical Neurons

    doi: 10.1371/journal.pone.0061787

    Figure Lengend Snippet: LY37 and selective mGluR2 agonist LY395756 (LY39) increased both surface and total protein level of GluA1 and GluA2 subunits in the cultured prefrontal neurons. (A and B) Treatment with LY37 or LY395756 significantly increased the total protein levels of both GluA1 and GluA2 subunits ( *p

    Article Snippet: LY395756 is a selective metabotropic glutamate ligand for mGluR2 and mGluR3 receptors with Ki values of 0.165 and 0.302 µM, respectively (Tocris Bioscience).

    Techniques: Cell Culture

    Selective mGluR2/3 antagonist LY341495 (LY34, 100 nM) completely blocked the effects of LY37 and LY395756 (LY39) on the protein levels of both GluA1 and GluA2 subunits. (A) LY37 signficantly increased the expression of GluA1 and GluA2 receptors, including surface, intracellular and total proteins (* p

    Journal: PLoS ONE

    Article Title: Group II Metabotropic Glutamate Receptor Agonist LY379268 Regulates AMPA Receptor Trafficking in Prefrontal Cortical Neurons

    doi: 10.1371/journal.pone.0061787

    Figure Lengend Snippet: Selective mGluR2/3 antagonist LY341495 (LY34, 100 nM) completely blocked the effects of LY37 and LY395756 (LY39) on the protein levels of both GluA1 and GluA2 subunits. (A) LY37 signficantly increased the expression of GluA1 and GluA2 receptors, including surface, intracellular and total proteins (* p

    Article Snippet: LY395756 is a selective metabotropic glutamate ligand for mGluR2 and mGluR3 receptors with Ki values of 0.165 and 0.302 µM, respectively (Tocris Bioscience).

    Techniques: Expressing

    Contribution of CCK B receptors to mitral cell excitation. A–B. CCK B -selective agonist CCK-4 evokes excitatory and suppressive spike responses. A. Histogram of spike counts over time (10 s bins) for a cell-attached spike recording from a mitral cell (CD-1 mouse) stimulated by perfusion with CCK-4 (horizontal bar). CCK-4 evoked a transient excitatory phase ( e ), followed by spike suppression ( s ), and after removal of stimulus there was a rebound excitation. B. Mean normalized spike rate for all mitral cell responses evoked by CCK-4 in CD-1 mice ( n = 7 cells, 4 excitatory, 2 mixed excitatory-suppressive, 1 suppressive). C–D. Stimulation by 1 µM CCK-8S causes spike excitation in CCK A knockout mice. C. Histogram of spike counts over time (20 s bins) for cell-attached spike recording from a mitral cell from a CCK A knockout mouse, showing excitation ( e ) in response to CCK stimulus (horizontal bar). D. Histogram of spike counts from the same cell after washout and reapplication of 1 µM CCK-8S (horizontal bar) in the presence of a CCK B -selective antagonist (5 µM LY 225910) which blocked spike excitation. E. Upper panel : mean spike rate (baseline subtracted) for mitral cells unresponsive to CCK-8S in the presence of LY225910 ( n = 9). Lower panel : mean normalized spike rate for excitatory spike responses evoked by CCK-8S in the presence of LY225910 ( n = 3 cells). All data from CD-1 mice. F–J. Inward current underlies spike excitation in the CCK A knockout mouse. F. Whole-cell voltage clamp recording from a mitral cell from a CCK A knockout mouse stimulated with 1 µM CCK-8S (horizontal bar), showing both slow inward current and an increase in EPSC activity, including currents underlying long lasting depolarizations (LLDs) [55] . G. Histogram of EPSC counts over time (20 s bins) for the trace in F , showing excitatory effect of CCK. H. Time course of slow inward current response to CCK for the trace in F , estimated by plotting baseline values for detected EPSCs (gray circles). Black line: smoothed curve obtained by averaging window of 8 data points. I. Whole-cell current clamp recording from same cell as in F , showing strong spike excitation caused by reapplication of 1 µM CCK-8S (horizontal bar). J. Histogram of spike counts over time (20 s bins) for the voltage trace in I , showing periods of spike frequency excitation ( e ) and suppression ( s ).

    Journal: PLoS ONE

    Article Title: Cholecystokinin: An Excitatory Modulator of Mitral/Tufted Cells in the Mouse Olfactory Bulb

    doi: 10.1371/journal.pone.0064170

    Figure Lengend Snippet: Contribution of CCK B receptors to mitral cell excitation. A–B. CCK B -selective agonist CCK-4 evokes excitatory and suppressive spike responses. A. Histogram of spike counts over time (10 s bins) for a cell-attached spike recording from a mitral cell (CD-1 mouse) stimulated by perfusion with CCK-4 (horizontal bar). CCK-4 evoked a transient excitatory phase ( e ), followed by spike suppression ( s ), and after removal of stimulus there was a rebound excitation. B. Mean normalized spike rate for all mitral cell responses evoked by CCK-4 in CD-1 mice ( n = 7 cells, 4 excitatory, 2 mixed excitatory-suppressive, 1 suppressive). C–D. Stimulation by 1 µM CCK-8S causes spike excitation in CCK A knockout mice. C. Histogram of spike counts over time (20 s bins) for cell-attached spike recording from a mitral cell from a CCK A knockout mouse, showing excitation ( e ) in response to CCK stimulus (horizontal bar). D. Histogram of spike counts from the same cell after washout and reapplication of 1 µM CCK-8S (horizontal bar) in the presence of a CCK B -selective antagonist (5 µM LY 225910) which blocked spike excitation. E. Upper panel : mean spike rate (baseline subtracted) for mitral cells unresponsive to CCK-8S in the presence of LY225910 ( n = 9). Lower panel : mean normalized spike rate for excitatory spike responses evoked by CCK-8S in the presence of LY225910 ( n = 3 cells). All data from CD-1 mice. F–J. Inward current underlies spike excitation in the CCK A knockout mouse. F. Whole-cell voltage clamp recording from a mitral cell from a CCK A knockout mouse stimulated with 1 µM CCK-8S (horizontal bar), showing both slow inward current and an increase in EPSC activity, including currents underlying long lasting depolarizations (LLDs) [55] . G. Histogram of EPSC counts over time (20 s bins) for the trace in F , showing excitatory effect of CCK. H. Time course of slow inward current response to CCK for the trace in F , estimated by plotting baseline values for detected EPSCs (gray circles). Black line: smoothed curve obtained by averaging window of 8 data points. I. Whole-cell current clamp recording from same cell as in F , showing strong spike excitation caused by reapplication of 1 µM CCK-8S (horizontal bar). J. Histogram of spike counts over time (20 s bins) for the voltage trace in I , showing periods of spike frequency excitation ( e ) and suppression ( s ).

    Article Snippet: We also evaluated the contribution of CCKB receptors by studying CCK responses in mitral cells from CCKA knockout mice . show that 1 µM CCK-8S could evoke spike excitation in the CCKA knockout, and that this response was abolished in the presence of a CCKB receptor-selective competitive antagonist, 5 µM LY225910 , .

    Techniques: Mouse Assay, Knock-Out, Activity Assay

    Contribution of CCK A receptors to mitral cell excitation. A–B. CCK evokes an excitatory inward current when CCK B receptors are blocked (compare to Figs. 6F–H). A. Upper panel : whole-cell voltage clamp recording from a mitral cell (CD-1 mouse) stimulated with 1 µM CCK-8S (lower horizontal bar), in the presence of 5 µM LY225910 (upper horizontal bar), a CCK B -selective antagonist. An inward current response was accompanied by increased EPSC activity (LLDs). Middle panel : histogram of EPSC counts over time (20 s bins) showing excitatory effect of CCK. Lower panel : time course of slow inward current response estimated by plotting baseline values for detected EPSCs (gray circles). Black line: smoothed curve obtained by averaging window of 8 data points. B. Upper panel : voltage clamp recording of inward current and EPSC from same cell as in A , stimulated with 1 µM CCK-8S (horizontal bar) after washout of LY225910, showing shorter inward current followed by outward current. Middle panel : histogram of EPSC counts over time (20 s bins) showing excitation followed by reduction in activity. Lower panel : Time course of slow inward/outward current response, estimated as in A. C. Histogram of spike counts over time (20 s bins) for cell-attached recording from a mitral cell (CD-1 mouse) showing excitation ( e ) in response to 300 nM CCK-8S (horizontal bar), in the presence of 1 µM LY225910 (pretreated slice). D. Histogram of spike counts over time (20 s bins) for cell-attached recording from a mitral cell from a CCK B knockout mouse showing excitation ( e ) and suppression ( s ) in response to 1 µM CCK-8S (horizontal bar). In this cell, spike rate rebounded noticeably after CCK washout. E. Upper panel : mean spike rate (baseline subtracted) for mitral cells from CCK B knockout mice unresponsive to CCK-8S ( n = 13). Lower panel : mean normalized spike rate for excitatory and excitatory-suppressive spike responses in CCK B knockout mice evoked by CCK-8S ( n = 3).

    Journal: PLoS ONE

    Article Title: Cholecystokinin: An Excitatory Modulator of Mitral/Tufted Cells in the Mouse Olfactory Bulb

    doi: 10.1371/journal.pone.0064170

    Figure Lengend Snippet: Contribution of CCK A receptors to mitral cell excitation. A–B. CCK evokes an excitatory inward current when CCK B receptors are blocked (compare to Figs. 6F–H). A. Upper panel : whole-cell voltage clamp recording from a mitral cell (CD-1 mouse) stimulated with 1 µM CCK-8S (lower horizontal bar), in the presence of 5 µM LY225910 (upper horizontal bar), a CCK B -selective antagonist. An inward current response was accompanied by increased EPSC activity (LLDs). Middle panel : histogram of EPSC counts over time (20 s bins) showing excitatory effect of CCK. Lower panel : time course of slow inward current response estimated by plotting baseline values for detected EPSCs (gray circles). Black line: smoothed curve obtained by averaging window of 8 data points. B. Upper panel : voltage clamp recording of inward current and EPSC from same cell as in A , stimulated with 1 µM CCK-8S (horizontal bar) after washout of LY225910, showing shorter inward current followed by outward current. Middle panel : histogram of EPSC counts over time (20 s bins) showing excitation followed by reduction in activity. Lower panel : Time course of slow inward/outward current response, estimated as in A. C. Histogram of spike counts over time (20 s bins) for cell-attached recording from a mitral cell (CD-1 mouse) showing excitation ( e ) in response to 300 nM CCK-8S (horizontal bar), in the presence of 1 µM LY225910 (pretreated slice). D. Histogram of spike counts over time (20 s bins) for cell-attached recording from a mitral cell from a CCK B knockout mouse showing excitation ( e ) and suppression ( s ) in response to 1 µM CCK-8S (horizontal bar). In this cell, spike rate rebounded noticeably after CCK washout. E. Upper panel : mean spike rate (baseline subtracted) for mitral cells from CCK B knockout mice unresponsive to CCK-8S ( n = 13). Lower panel : mean normalized spike rate for excitatory and excitatory-suppressive spike responses in CCK B knockout mice evoked by CCK-8S ( n = 3).

    Article Snippet: We also evaluated the contribution of CCKB receptors by studying CCK responses in mitral cells from CCKA knockout mice . show that 1 µM CCK-8S could evoke spike excitation in the CCKA knockout, and that this response was abolished in the presence of a CCKB receptor-selective competitive antagonist, 5 µM LY225910 , .

    Techniques: Activity Assay, Knock-Out, Mouse Assay

    NMDA receptor antagonism switched the effects of experimenter-administered nicotine on brain reward systems from stimulatory to inhibitory. ( a ) Rats ( n =9) were pretreated with saline or LY235959 (1 mg/kg), and subsequently received saline or nicotine

    Journal:

    Article Title: NMDA receptors regulate nicotine-enhanced brain reward function and intravenous nicotine self-administration: Role of the ventral tegmental area and central nucleus of the amygdala

    doi: 10.1038/npp.2008.58

    Figure Lengend Snippet: NMDA receptor antagonism switched the effects of experimenter-administered nicotine on brain reward systems from stimulatory to inhibitory. ( a ) Rats ( n =9) were pretreated with saline or LY235959 (1 mg/kg), and subsequently received saline or nicotine

    Article Snippet: For intra-CeA or intra-VTA administration, LY235959 was dissolved in sterile saline, and administered bilaterally in a volume of 0.5 μl/side delivered over 66 sec using stainless-steel injectors.

    Techniques:

    The effects of ACPA and LY320135 on β -band activity in mEC layer V. (a) Example traces from layer V showing β -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 15–29 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of ACPA and LY320135 on β -band activity in mEC layer V. (a) Example traces from layer V showing β -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 15–29 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques: Activity Assay

    The effects of ACPA and LY320135 on β -band activity in mEC layer II. (a) Example traces from layer II showing β -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 15–29 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of ACPA and LY320135 on β -band activity in mEC layer II. (a) Example traces from layer II showing β -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 15–29 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques: Activity Assay

    The effects of LY320135 on sIPSCs in mEC layer V. (a) Recording from a layer V neurone under control conditions and (b) in the presence of LY320135 (500 nM). (c) Cumulative probability plot for sIPSC amplitude under control (black) and LY320135 (red) conditions. (d) Cumulative probability plot for sIPSC IEI under control (black) and LY320135 (red) conditions. Scale bars 2000 milliseconds × 250 pA.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of LY320135 on sIPSCs in mEC layer V. (a) Recording from a layer V neurone under control conditions and (b) in the presence of LY320135 (500 nM). (c) Cumulative probability plot for sIPSC amplitude under control (black) and LY320135 (red) conditions. (d) Cumulative probability plot for sIPSC IEI under control (black) and LY320135 (red) conditions. Scale bars 2000 milliseconds × 250 pA.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques:

    The effects of LY320135 on sIPSCs in mEC layer II. (a) Recording from a layer II neurone under control conditions and (b) in the presence of LY320135 (500 nM). (c) Cumulative probability plot for sIPSC amplitude under control (black) and LY320135 (red) conditions. (d) Cumulative probability plot for sIPSC IEI under control (black) and LY320135 (red) conditions. Scale bars 500 milliseconds × 250 pA.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of LY320135 on sIPSCs in mEC layer II. (a) Recording from a layer II neurone under control conditions and (b) in the presence of LY320135 (500 nM). (c) Cumulative probability plot for sIPSC amplitude under control (black) and LY320135 (red) conditions. (d) Cumulative probability plot for sIPSC IEI under control (black) and LY320135 (red) conditions. Scale bars 500 milliseconds × 250 pA.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques:

    The effects of ACPA and LY320135 on γ -band activity in mEC layer V. (a) Example traces from layer V showing γ -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) was applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), or LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 30–90 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of ACPA and LY320135 on γ -band activity in mEC layer V. (a) Example traces from layer V showing γ -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) was applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), or LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 30–90 Hz. Scale bar = 200 milliseconds × 50 μ V.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques: Activity Assay

    The effects of ACPA and LY320135 on γ -band activity in mEC layer II. (a) Example traces from layer II showing γ -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 30–90 Hz. Scale bar = 200 milliseconds × 100 μ V.

    Journal: Neural Plasticity

    Article Title: Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex

    doi: 10.1155/2008/808564

    Figure Lengend Snippet: The effects of ACPA and LY320135 on γ -band activity in mEC layer II. (a) Example traces from layer II showing γ -oscillations under conditions in which ACPA (10 μ M) or LY320135 (500 nM) were applied. (b) Plot of power spectral density during drug application (filtered between 2–100 Hz). Control (black line), ACPA (red line), LY320135 (blue line). (c) Similar plot to (b) bandpass filtered between 30–90 Hz. Scale bar = 200 milliseconds × 100 μ V.

    Article Snippet: LY320135 and ACPA were obtained from Tocris Cookson (UK).

    Techniques: Activity Assay

    Effects of ZJ43 and (R,S)-2-phosphono-methylpentanedioic acid (2-PMPA) on dizocilpine (MK-801)-induced cognitive deficit in the novel object recognition test. C57BL mice were injected (INJ) with by MK-801 (0.2 mg kg −1 , intraperitoneally (i.p.)) or saline 20 min after i.p. injection with: ( a ) saline (s), ZJ43 (50, 100 or 150 mg kg −1 ) or 150 mg kg −1 ZJ43 with LY341495 (1 mg kg −1 ); ( b ) 2-PMPA (10, 50, 100 mg kg −1 ), 100 mg kg −1 2-PMPA with LY341495 (1 mg kg −1 ), or LY341495 (1 mg kg −1 ) and 30 min later placed in a chamber with two identical objects for a 10-min acquisition session (AS) 30 min. Mice were tested with one original and one novel object in a recognition session (RS) 90 min after the AS. The recognition index for the AS was calculated as: (time exploring one of the objects/ time exploring both the objects) × 100. For the RS, the recognition index was calculated as: (time exploring the novel object/ time exploring the familiar and the novel object) × 100. ( a ) Saline-treated mice attended the novel object about twice as much as the familiar object. MK801 given before the AS blocked memory of the familiar object during the RS. ZJ43 (100 and 150 mg kg −1 ) blocked the effects of MK-801. The effect of ZJ43 (150 mg kg −1 ) on MK-801 was reversed by 1 mg kg −1 of the metabotropic glutamate receptor 2/3 antagonist LY341495. ZJ43 (100 mg kg −1 ) was not effective in blocking the MK-801 effect when given immediately after the AS. n =9–24 mice per group. ( b ) 2-PMPA dose-response on MK-801-induced cognitive deficits in the novel object recognition test. 2-PMPA (100 and 150 mg kg −1 ) blocked the effect of MK-801. LY341495 (1 mg kg −1 ) blocked the effect of 2-PMPA (100 mg kg −1 ) on MK-801. n =5–24 mice per group. Data for the saline (s-s) and saline+MK-801 (s MK) are the same as in a and b , respectively.

    Journal: Translational Psychiatry

    Article Title: NAAG peptidase inhibitors block cognitive deficit induced by MK-801 and motor activation induced by d-amphetamine in animal models of schizophrenia

    doi: 10.1038/tp.2012.68

    Figure Lengend Snippet: Effects of ZJ43 and (R,S)-2-phosphono-methylpentanedioic acid (2-PMPA) on dizocilpine (MK-801)-induced cognitive deficit in the novel object recognition test. C57BL mice were injected (INJ) with by MK-801 (0.2 mg kg −1 , intraperitoneally (i.p.)) or saline 20 min after i.p. injection with: ( a ) saline (s), ZJ43 (50, 100 or 150 mg kg −1 ) or 150 mg kg −1 ZJ43 with LY341495 (1 mg kg −1 ); ( b ) 2-PMPA (10, 50, 100 mg kg −1 ), 100 mg kg −1 2-PMPA with LY341495 (1 mg kg −1 ), or LY341495 (1 mg kg −1 ) and 30 min later placed in a chamber with two identical objects for a 10-min acquisition session (AS) 30 min. Mice were tested with one original and one novel object in a recognition session (RS) 90 min after the AS. The recognition index for the AS was calculated as: (time exploring one of the objects/ time exploring both the objects) × 100. For the RS, the recognition index was calculated as: (time exploring the novel object/ time exploring the familiar and the novel object) × 100. ( a ) Saline-treated mice attended the novel object about twice as much as the familiar object. MK801 given before the AS blocked memory of the familiar object during the RS. ZJ43 (100 and 150 mg kg −1 ) blocked the effects of MK-801. The effect of ZJ43 (150 mg kg −1 ) on MK-801 was reversed by 1 mg kg −1 of the metabotropic glutamate receptor 2/3 antagonist LY341495. ZJ43 (100 mg kg −1 ) was not effective in blocking the MK-801 effect when given immediately after the AS. n =9–24 mice per group. ( b ) 2-PMPA dose-response on MK-801-induced cognitive deficits in the novel object recognition test. 2-PMPA (100 and 150 mg kg −1 ) blocked the effect of MK-801. LY341495 (1 mg kg −1 ) blocked the effect of 2-PMPA (100 mg kg −1 ) on MK-801. n =5–24 mice per group. Data for the saline (s-s) and saline+MK-801 (s MK) are the same as in a and b , respectively.

    Article Snippet: Novel object recognition test Novel object recognition is widely used test for assessing the efficacy of therapeutic approaches to schizophrenia in animal models., , , , , , , , , , C57BL mice were placed individually in a 32 × 30 cm box with beige walls for 5 min habituation followed by injection with saline or ZJ43 (before or after acquisition) or 2-PMPA with and without LY341495 and returned to the chamber.

    Techniques: Mouse Assay, Injection, Blocking Assay

    Effects of ZJ43 treatment after onset of d -amphetamine (AMPH)-induced motor activation in C57BL mice. ( a ) Time course of AMPH-induced motor activation presented in 5-min intervals. To test the efficacy of N -acetylaspartylglutamate (NAAG) peptidase inhibitor, ZJ43, in the reversal of ongoing AMPH- induced motor activation, animals were habituated in the open field chamber (0–30 min), injected (intraperitoneally (i.p.)) with saline or 3 mg kg −1 AMPH at the 30 min time point in this figure. Saline or ZJ43 (150 mg kg −1 , i.p.), ZJ43 with LY341495 or LY342495 with saline were injected 10 min later at the 40 min time point. n =14–16 animals/group. Coinjection of LY341495 with AMPH did not significantly affect the induced motor activation but did block the effect of ZJ43 on AMPH treatment. ( b ) Mice received AMPH with or without LY341495 injected at the 30 min time point as in Figure 2a . Saline or ZJ43 was injected 10, 15, 20 and 25 min after AMPH. The distances travelled were measured from the time point 5 min after the second injection to the 100 min time point shown in Figure 2a , resulting in distance traveled data over 55, 50, 45 and 40 min intervals for the 10, 15, 20 and 25 min post-MPH treatment groups, respectively. Distance travelled is compared between saline and ZJ43 treatments at each post-AMPH treatment time.

    Journal: Translational Psychiatry

    Article Title: NAAG peptidase inhibitors block cognitive deficit induced by MK-801 and motor activation induced by d-amphetamine in animal models of schizophrenia

    doi: 10.1038/tp.2012.68

    Figure Lengend Snippet: Effects of ZJ43 treatment after onset of d -amphetamine (AMPH)-induced motor activation in C57BL mice. ( a ) Time course of AMPH-induced motor activation presented in 5-min intervals. To test the efficacy of N -acetylaspartylglutamate (NAAG) peptidase inhibitor, ZJ43, in the reversal of ongoing AMPH- induced motor activation, animals were habituated in the open field chamber (0–30 min), injected (intraperitoneally (i.p.)) with saline or 3 mg kg −1 AMPH at the 30 min time point in this figure. Saline or ZJ43 (150 mg kg −1 , i.p.), ZJ43 with LY341495 or LY342495 with saline were injected 10 min later at the 40 min time point. n =14–16 animals/group. Coinjection of LY341495 with AMPH did not significantly affect the induced motor activation but did block the effect of ZJ43 on AMPH treatment. ( b ) Mice received AMPH with or without LY341495 injected at the 30 min time point as in Figure 2a . Saline or ZJ43 was injected 10, 15, 20 and 25 min after AMPH. The distances travelled were measured from the time point 5 min after the second injection to the 100 min time point shown in Figure 2a , resulting in distance traveled data over 55, 50, 45 and 40 min intervals for the 10, 15, 20 and 25 min post-MPH treatment groups, respectively. Distance travelled is compared between saline and ZJ43 treatments at each post-AMPH treatment time.

    Article Snippet: Novel object recognition test Novel object recognition is widely used test for assessing the efficacy of therapeutic approaches to schizophrenia in animal models., , , , , , , , , , C57BL mice were placed individually in a 32 × 30 cm box with beige walls for 5 min habituation followed by injection with saline or ZJ43 (before or after acquisition) or 2-PMPA with and without LY341495 and returned to the chamber.

    Techniques: Activation Assay, Mouse Assay, Injection, Blocking Assay

    Receptor subtype-specific effects of group I mGluR activation on locomotor-related motoneuron output. A : time course plots showing that the mGluR1 antagonist LY367385 (50 μM) blocked DHPG (5 μM)-mediated effects on locomotor burst amplitude

    Journal: Journal of Neurophysiology

    Article Title: Activation of group I metabotropic glutamate receptors modulates locomotor-related motoneuron output in mice

    doi: 10.1152/jn.01037.2010

    Figure Lengend Snippet: Receptor subtype-specific effects of group I mGluR activation on locomotor-related motoneuron output. A : time course plots showing that the mGluR1 antagonist LY367385 (50 μM) blocked DHPG (5 μM)-mediated effects on locomotor burst amplitude

    Article Snippet: Pharmacological agents used included the following: NMDA, 5-HT, dopamine, strychnine [(−)-strychnine], and bicuculline [1( S ),9( R )-(−)-bicuculline methiodide] purchased from Sigma-Aldrich (St Louis, MO); and DHPG [( S )-3,5-dihydroxyphenylglycine], LY367385 [( S )-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid], MPEP [2-methyl-6-(phenylethynyl)pyridine hydrochloride], and tetrodotoxin (TTX) purchased from Tocris Bioscience (Bristrol, UK).

    Techniques: Activation Assay