HY-123252 Search Results


gsk2194069  (MedChemExpress)
93
MedChemExpress gsk2194069
A Scatter plots show example correlations between relative lipid abundance and S phase percentage over the different inhibitor treatments and time points. Line indicates linear fit. Dots are labeled based on inhibitor treatment and time point. B Left: Nodes of the network are color-coded based on the correlations between relative lipid abundance and S phase percentage. Right: For orientation the lipid map shows the nodes of the network color-coded by lipid classes. A , B Data are combined of at least three independent experiments and shown as mean. C Top: Hierarchical clustering of lipid-mRNA abundance correlations. Rows: 250 lipids, columns: 3739 differentially expressed genes after C75 treatment. Bottom: Rug plot represents the distribution of ATF4-dependent genes and the gray area shows the percentage of ATF4-dependent genes per gene cluster. 3739 genes are divided into 11 gene clusters (clustergram - MATLAB) based on their lipid correlation. Clusters 5 and 6 are significantly enriched for ATF-dependent genes as calculated by two-sided Fisher’s exact test. D – F Example correlations of selected genes with 250 lipids color-coded on the circular network. Different clusters show different distribution of correlations across the network. G Bar plot shows fold enrichment for Gene Ontology (GO) Terms (BP direct) among genes significantly upregulated in cells treated with C75 for 3 h at 9 h after EGF release (mRNA sequencing data, significant in at least 3 replicates, p.adj <0.05, filtered for increased expression in starved cells and at least twofold upregulated compared to DMSO control). P values were calculated using EASE score (Fisher’s Exact test). Processes sorted by false discovery rate (FDR)–adjusted P value. Redundant processes omitted. H Volcano plot shows differentially regulated genes after 3 h of C75 treatment. Differentially expressed genes (log 2 (fold-change) | > 1, p.adj. <0.014) in blue (genes associated with the ER stress pathway based on GO terms) or magenta (ATF4-dependent genes ) or both (blue-magenta). CDKN1A (p21) is highlighted in red as the ER stress-cell cycle link. G , H P. adj. values are Benjamini-Hochberg adjusted p values calculated using the two-sided Wald test. Inhibitor concentrations used: C75 (30 µM), <t>GSK2194069</t> (50 µM), SCDi (32 µM). FC, fold-change.
Gsk2194069, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gsk2194069/product/MedChemExpress
Average 93 stars, based on 1 article reviews
gsk2194069 - by Bioz Stars, 2026-03
93/100 stars
  Buy from Supplier

Image Search Results


A Scatter plots show example correlations between relative lipid abundance and S phase percentage over the different inhibitor treatments and time points. Line indicates linear fit. Dots are labeled based on inhibitor treatment and time point. B Left: Nodes of the network are color-coded based on the correlations between relative lipid abundance and S phase percentage. Right: For orientation the lipid map shows the nodes of the network color-coded by lipid classes. A , B Data are combined of at least three independent experiments and shown as mean. C Top: Hierarchical clustering of lipid-mRNA abundance correlations. Rows: 250 lipids, columns: 3739 differentially expressed genes after C75 treatment. Bottom: Rug plot represents the distribution of ATF4-dependent genes and the gray area shows the percentage of ATF4-dependent genes per gene cluster. 3739 genes are divided into 11 gene clusters (clustergram - MATLAB) based on their lipid correlation. Clusters 5 and 6 are significantly enriched for ATF-dependent genes as calculated by two-sided Fisher’s exact test. D – F Example correlations of selected genes with 250 lipids color-coded on the circular network. Different clusters show different distribution of correlations across the network. G Bar plot shows fold enrichment for Gene Ontology (GO) Terms (BP direct) among genes significantly upregulated in cells treated with C75 for 3 h at 9 h after EGF release (mRNA sequencing data, significant in at least 3 replicates, p.adj <0.05, filtered for increased expression in starved cells and at least twofold upregulated compared to DMSO control). P values were calculated using EASE score (Fisher’s Exact test). Processes sorted by false discovery rate (FDR)–adjusted P value. Redundant processes omitted. H Volcano plot shows differentially regulated genes after 3 h of C75 treatment. Differentially expressed genes (log 2 (fold-change) | > 1, p.adj. <0.014) in blue (genes associated with the ER stress pathway based on GO terms) or magenta (ATF4-dependent genes ) or both (blue-magenta). CDKN1A (p21) is highlighted in red as the ER stress-cell cycle link. G , H P. adj. values are Benjamini-Hochberg adjusted p values calculated using the two-sided Wald test. Inhibitor concentrations used: C75 (30 µM), GSK2194069 (50 µM), SCDi (32 µM). FC, fold-change.

Journal: Nature Communications

Article Title: A fast-acting lipid checkpoint in G1 prevents mitotic defects

doi: 10.1038/s41467-024-46696-9

Figure Lengend Snippet: A Scatter plots show example correlations between relative lipid abundance and S phase percentage over the different inhibitor treatments and time points. Line indicates linear fit. Dots are labeled based on inhibitor treatment and time point. B Left: Nodes of the network are color-coded based on the correlations between relative lipid abundance and S phase percentage. Right: For orientation the lipid map shows the nodes of the network color-coded by lipid classes. A , B Data are combined of at least three independent experiments and shown as mean. C Top: Hierarchical clustering of lipid-mRNA abundance correlations. Rows: 250 lipids, columns: 3739 differentially expressed genes after C75 treatment. Bottom: Rug plot represents the distribution of ATF4-dependent genes and the gray area shows the percentage of ATF4-dependent genes per gene cluster. 3739 genes are divided into 11 gene clusters (clustergram - MATLAB) based on their lipid correlation. Clusters 5 and 6 are significantly enriched for ATF-dependent genes as calculated by two-sided Fisher’s exact test. D – F Example correlations of selected genes with 250 lipids color-coded on the circular network. Different clusters show different distribution of correlations across the network. G Bar plot shows fold enrichment for Gene Ontology (GO) Terms (BP direct) among genes significantly upregulated in cells treated with C75 for 3 h at 9 h after EGF release (mRNA sequencing data, significant in at least 3 replicates, p.adj <0.05, filtered for increased expression in starved cells and at least twofold upregulated compared to DMSO control). P values were calculated using EASE score (Fisher’s Exact test). Processes sorted by false discovery rate (FDR)–adjusted P value. Redundant processes omitted. H Volcano plot shows differentially regulated genes after 3 h of C75 treatment. Differentially expressed genes (log 2 (fold-change) | > 1, p.adj. <0.014) in blue (genes associated with the ER stress pathway based on GO terms) or magenta (ATF4-dependent genes ) or both (blue-magenta). CDKN1A (p21) is highlighted in red as the ER stress-cell cycle link. G , H P. adj. values are Benjamini-Hochberg adjusted p values calculated using the two-sided Wald test. Inhibitor concentrations used: C75 (30 µM), GSK2194069 (50 µM), SCDi (32 µM). FC, fold-change.

Article Snippet: Chemicals used were C75 (Sigma Aldrich), TOFA (5-(tetradecyloxy)-2-furoic acid), acetyl-CoA carboxylase inhibitor (Abcam, ab141578), Triascin C (Enzo, BML-EI218-100), Bromoenol Lactone (Cayman Chemical, 70700), Etomoxir (Calbiochem/MilliporeSigma), T-863 (Cayman Chemical, 25807), SB 204990 (Cayman Chemical, 15245), Cerulenin (Santa Cruz Biotechnology), GSK2194069 (Sigma Aldrich), CAY10566, GSK2606414 (both Cayman Chemical), Tunicamycin (Cayman Chemical), MMS (Santa Cruz Biotechnology), NCS (Sigma Aldrich), Torin2, Nutlin-3 (both Medchemexpress), DMSO (Sigma Aldrich).

Techniques: Labeling, Sequencing, Expressing, Control

A EGF-released MCF-10A cells (4 h) treated with DMSO or C75. Sample immunofluorescence images for nuclei (Hoechst), p21, and Cyclin D are shown. Scale bar: 10 µm. Data are representative of at least seven independent experiments. B Quantification of nuclear protein levels as shown in ( A ). Data are shown as mean ± SD from at least seven independent experiments, n > 20,000 cells per condition. C EGF-released cells (4 h) treated with indicated inhibitors. Blotted for Cyclin D, p21, and β-actin (loading control). Data are representative of three independent experiments. D Nuclear p21 and Cyclin D protein levels after EGF release and treatment with DMSO or C75 measured by immunofluorescence. Data are representative of at least two independent experiments (data points are means of two technical replicates), n > 17,000 cells per condition. E mRNA levels of CDKN1A (p21) and CCND1 (Cyclin D) measured by qRT-PCR after treatment with DMSO or C75 and normalized to unreleased cells. Data are from at least two independent experiments. F Cyclin D and p21 nuclear protein levels measured by immunofluorescence after 8 h of EGF release in the presence of DMSO or Tunicamycin. Data are from two independent experiments, n > 12,000 cells per condition. B , E, F P values calculated using two-tailed Paired t test. Inhibitor concentrations used unless indicated otherwise: C75 (15 µM), GSK2194069 (50 µM), Tunicamycin (10 µg/ml), Nutlin-3 (10 µM), Torin2 (500 nM). Source data are provided as Source data file.

Journal: Nature Communications

Article Title: A fast-acting lipid checkpoint in G1 prevents mitotic defects

doi: 10.1038/s41467-024-46696-9

Figure Lengend Snippet: A EGF-released MCF-10A cells (4 h) treated with DMSO or C75. Sample immunofluorescence images for nuclei (Hoechst), p21, and Cyclin D are shown. Scale bar: 10 µm. Data are representative of at least seven independent experiments. B Quantification of nuclear protein levels as shown in ( A ). Data are shown as mean ± SD from at least seven independent experiments, n > 20,000 cells per condition. C EGF-released cells (4 h) treated with indicated inhibitors. Blotted for Cyclin D, p21, and β-actin (loading control). Data are representative of three independent experiments. D Nuclear p21 and Cyclin D protein levels after EGF release and treatment with DMSO or C75 measured by immunofluorescence. Data are representative of at least two independent experiments (data points are means of two technical replicates), n > 17,000 cells per condition. E mRNA levels of CDKN1A (p21) and CCND1 (Cyclin D) measured by qRT-PCR after treatment with DMSO or C75 and normalized to unreleased cells. Data are from at least two independent experiments. F Cyclin D and p21 nuclear protein levels measured by immunofluorescence after 8 h of EGF release in the presence of DMSO or Tunicamycin. Data are from two independent experiments, n > 12,000 cells per condition. B , E, F P values calculated using two-tailed Paired t test. Inhibitor concentrations used unless indicated otherwise: C75 (15 µM), GSK2194069 (50 µM), Tunicamycin (10 µg/ml), Nutlin-3 (10 µM), Torin2 (500 nM). Source data are provided as Source data file.

Article Snippet: Chemicals used were C75 (Sigma Aldrich), TOFA (5-(tetradecyloxy)-2-furoic acid), acetyl-CoA carboxylase inhibitor (Abcam, ab141578), Triascin C (Enzo, BML-EI218-100), Bromoenol Lactone (Cayman Chemical, 70700), Etomoxir (Calbiochem/MilliporeSigma), T-863 (Cayman Chemical, 25807), SB 204990 (Cayman Chemical, 15245), Cerulenin (Santa Cruz Biotechnology), GSK2194069 (Sigma Aldrich), CAY10566, GSK2606414 (both Cayman Chemical), Tunicamycin (Cayman Chemical), MMS (Santa Cruz Biotechnology), NCS (Sigma Aldrich), Torin2, Nutlin-3 (both Medchemexpress), DMSO (Sigma Aldrich).

Techniques: Immunofluorescence, Control, Quantitative RT-PCR, Two Tailed Test

A Schematic highlighting Cyclin-dependent kinase (CDK) signaling in G1. B Histogram of Rb(p-S807/S811) signal of cells treated with C75 or DMSO after EGF release (20 h). Percentages are shown as mean ± SD of four independent experiments, n > 17,000 cells per condition. C Dose response of percent Rb(p-S807/S811) positive cells treated with C75 normalized to DMSO treatment after EGF release (20 h). Data are from at least three independent experiments, n > 17,000 cells per condition. D Percentage of Rb(p-S807/S811) positive cells treated with DMSO or C75 after EGF release (20 h). GM (growth media): 5% serum. Data are shown as mean ± SD from three independent experiments, n > 15,000 cells per condition. E Percentage of Rb(p-S807/S811) positive cells treated with DMSO or C75 after EGF release (20 h). PA-BSA indicates the presence of Palmitate complexed to BSA. NaCl-BSA is the control treatment. Data are shown as mean ± SD from three independent experiments, n > 15,000 cells per condition. F Histogram of Rb(p-S807/S811) signal of cells treated with Tunicamycin or DMSO and EGF-released (20 h). Percentages are shown as mean ± SD of at least three independent experiments, n > 15,000 cells per condition. G Percent of Rb(p-S807/S811) positive cells transfected with sicontrol (sictrl) or sip21 and treated with DMSO or C75. Data are shown as mean ± SD from three independent experiments, n > 14,000 cells per condition. H Schematic depicting the workflow of treatments. Histogram of Rb(p-S807/S811) signal of cells treated with different inhibitors. Percentages are from two independent experiments and shown as mean ± SD, n > 20,000 cells per condition. I Schematic summary of the findings: Lipidome analysis shows the balance of increased unsaturated lipids (blue) and decreased saturated lipids (red) to overcome the lipid checkpoint in G1 (outlook for S/G2/M is extrapolated based on the G1 data). Lipid checkpoint engagement mediated by PERK-mediated ER stress feeds back to cell-cycle signaling by increasing p21 levels, decreasing Cyclin D and Rb (p-S807/S811) causing a cell-cycle delay. D , E , G P values calculated using two-tailed Paired t test. Inhibitor concentrations used unless indicated otherwise: C75 (15 µM), GSK2194069 (50 µM), Tunicamycin (10 µg/ml), Palmitate (5 µM). Source data are provided as Source data file.

Journal: Nature Communications

Article Title: A fast-acting lipid checkpoint in G1 prevents mitotic defects

doi: 10.1038/s41467-024-46696-9

Figure Lengend Snippet: A Schematic highlighting Cyclin-dependent kinase (CDK) signaling in G1. B Histogram of Rb(p-S807/S811) signal of cells treated with C75 or DMSO after EGF release (20 h). Percentages are shown as mean ± SD of four independent experiments, n > 17,000 cells per condition. C Dose response of percent Rb(p-S807/S811) positive cells treated with C75 normalized to DMSO treatment after EGF release (20 h). Data are from at least three independent experiments, n > 17,000 cells per condition. D Percentage of Rb(p-S807/S811) positive cells treated with DMSO or C75 after EGF release (20 h). GM (growth media): 5% serum. Data are shown as mean ± SD from three independent experiments, n > 15,000 cells per condition. E Percentage of Rb(p-S807/S811) positive cells treated with DMSO or C75 after EGF release (20 h). PA-BSA indicates the presence of Palmitate complexed to BSA. NaCl-BSA is the control treatment. Data are shown as mean ± SD from three independent experiments, n > 15,000 cells per condition. F Histogram of Rb(p-S807/S811) signal of cells treated with Tunicamycin or DMSO and EGF-released (20 h). Percentages are shown as mean ± SD of at least three independent experiments, n > 15,000 cells per condition. G Percent of Rb(p-S807/S811) positive cells transfected with sicontrol (sictrl) or sip21 and treated with DMSO or C75. Data are shown as mean ± SD from three independent experiments, n > 14,000 cells per condition. H Schematic depicting the workflow of treatments. Histogram of Rb(p-S807/S811) signal of cells treated with different inhibitors. Percentages are from two independent experiments and shown as mean ± SD, n > 20,000 cells per condition. I Schematic summary of the findings: Lipidome analysis shows the balance of increased unsaturated lipids (blue) and decreased saturated lipids (red) to overcome the lipid checkpoint in G1 (outlook for S/G2/M is extrapolated based on the G1 data). Lipid checkpoint engagement mediated by PERK-mediated ER stress feeds back to cell-cycle signaling by increasing p21 levels, decreasing Cyclin D and Rb (p-S807/S811) causing a cell-cycle delay. D , E , G P values calculated using two-tailed Paired t test. Inhibitor concentrations used unless indicated otherwise: C75 (15 µM), GSK2194069 (50 µM), Tunicamycin (10 µg/ml), Palmitate (5 µM). Source data are provided as Source data file.

Article Snippet: Chemicals used were C75 (Sigma Aldrich), TOFA (5-(tetradecyloxy)-2-furoic acid), acetyl-CoA carboxylase inhibitor (Abcam, ab141578), Triascin C (Enzo, BML-EI218-100), Bromoenol Lactone (Cayman Chemical, 70700), Etomoxir (Calbiochem/MilliporeSigma), T-863 (Cayman Chemical, 25807), SB 204990 (Cayman Chemical, 15245), Cerulenin (Santa Cruz Biotechnology), GSK2194069 (Sigma Aldrich), CAY10566, GSK2606414 (both Cayman Chemical), Tunicamycin (Cayman Chemical), MMS (Santa Cruz Biotechnology), NCS (Sigma Aldrich), Torin2, Nutlin-3 (both Medchemexpress), DMSO (Sigma Aldrich).

Techniques: Control, Transfection, Two Tailed Test