3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt  (Millipore)

 
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    Structured Review

    Millipore 3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt
    POMHEX selectively induces energy stress, inhibits proliferation, and triggers apoptosis in ENO1 -deleted glioma cells. ENO1 -deleted (D423, red), ENO1 -isogenically rescued (D423 ENO1, blue), and ENO1 -WT (LN319, grey) glioma cells were treated with the Enolase inhibitor POMHEX for 72 hours. Cells were harvested for protein lysates and polar metabolites. a . ENO1 -deleted cells experience dose-dependent increase in stress response markers (phosphorylated T346 NDRG1, S73 c-Jun), decrease in proliferation (phosphorylated Histone H3, PLK1), and increase in cell death (cleaved caspsase-3), as indicated by western blot. Such effects are exclusive to ENO1 -deleted cells (left, red) and are absent in ENO1 -WT cells (middle, blue; right, grey). b. Lactate levels were measured by 1 H NMR with the integral of 1.34 ppm doublet normalized to <t>3-(trimethylsilyl)propionic-2,2,3,3-d4</t> acid standard and expressed as % of CT [(n=2(CT), mean of n=1 (treated biological replicates)]. A dose-dependent decrease in lactate levels is unique to ENO1 -deleted, but not ENO1 -WT, glioma cells. c. Glycerate levels were used as a marker of Enolase inhibition and were measured by mass spectrometry. Values are expressed as % of CT [(n = 4(CT), mean of n = 2 (treated biological replicates)]. A dose-dependent increase in glycerate levels was observed in ENO1 -deleted but not ENO1 -WT glioma cells. d-e. Phosphocreatine/creatine ratio and pyrophosphate (PPi) levels quantified via mass spectrometry were used as measures of energy stress. The dose-dependent decrease in phosphocreatine to creatine ratio ( d ) and increase in PPi ( e ) in response to POMHEX treatment is specific to ENO1 -deleted glioma cells. Both measurements are expressed as a % of CT [N = 4(CT), mean of N = 2 (treated biological replicates)]. f . Treatment with POMHEX results in depletion of anaplerotic substrates. Top: metabolic map showing relative increases (red) and decreases (blue) of relevant metabolites in glycolysis, hexosamine biosynthesis pathway, non-oxidative pentose phosphate pathway, and TCA cycle in ENO1 -deleted (D423) cells. Bottom: heat map of relevant metabolites in ENO1 -deleted (D423), ENO1 -heterozygous deleted (D502, U343), and ENO1 -WT (LN319) glioma cells. A decrease in TCA metabolites is observed across all cell lines treated with POMHEX, Relative abundance is expressed as area-under-the-curve calculations of metabolite levels obtained from dose-response POMHEX treatment.
    3 Trimethylsilyl Propionic 2 2 3 3 D4 Acid Sodium Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt/product/Millipore
    Average 98 stars, based on 13 article reviews
    Price from $9.99 to $1999.99
    3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt - by Bioz Stars, 2022-11
    98/100 stars

    Images

    1) Product Images from "An Enolase Inhibitor for the Targeted Treatment of ENO1-Deleted Cancers"

    Article Title: An Enolase Inhibitor for the Targeted Treatment of ENO1-Deleted Cancers

    Journal: Nature metabolism

    doi: 10.1038/s42255-020-00313-3

    POMHEX selectively induces energy stress, inhibits proliferation, and triggers apoptosis in ENO1 -deleted glioma cells. ENO1 -deleted (D423, red), ENO1 -isogenically rescued (D423 ENO1, blue), and ENO1 -WT (LN319, grey) glioma cells were treated with the Enolase inhibitor POMHEX for 72 hours. Cells were harvested for protein lysates and polar metabolites. a . ENO1 -deleted cells experience dose-dependent increase in stress response markers (phosphorylated T346 NDRG1, S73 c-Jun), decrease in proliferation (phosphorylated Histone H3, PLK1), and increase in cell death (cleaved caspsase-3), as indicated by western blot. Such effects are exclusive to ENO1 -deleted cells (left, red) and are absent in ENO1 -WT cells (middle, blue; right, grey). b. Lactate levels were measured by 1 H NMR with the integral of 1.34 ppm doublet normalized to 3-(trimethylsilyl)propionic-2,2,3,3-d4 acid standard and expressed as % of CT [(n=2(CT), mean of n=1 (treated biological replicates)]. A dose-dependent decrease in lactate levels is unique to ENO1 -deleted, but not ENO1 -WT, glioma cells. c. Glycerate levels were used as a marker of Enolase inhibition and were measured by mass spectrometry. Values are expressed as % of CT [(n = 4(CT), mean of n = 2 (treated biological replicates)]. A dose-dependent increase in glycerate levels was observed in ENO1 -deleted but not ENO1 -WT glioma cells. d-e. Phosphocreatine/creatine ratio and pyrophosphate (PPi) levels quantified via mass spectrometry were used as measures of energy stress. The dose-dependent decrease in phosphocreatine to creatine ratio ( d ) and increase in PPi ( e ) in response to POMHEX treatment is specific to ENO1 -deleted glioma cells. Both measurements are expressed as a % of CT [N = 4(CT), mean of N = 2 (treated biological replicates)]. f . Treatment with POMHEX results in depletion of anaplerotic substrates. Top: metabolic map showing relative increases (red) and decreases (blue) of relevant metabolites in glycolysis, hexosamine biosynthesis pathway, non-oxidative pentose phosphate pathway, and TCA cycle in ENO1 -deleted (D423) cells. Bottom: heat map of relevant metabolites in ENO1 -deleted (D423), ENO1 -heterozygous deleted (D502, U343), and ENO1 -WT (LN319) glioma cells. A decrease in TCA metabolites is observed across all cell lines treated with POMHEX, Relative abundance is expressed as area-under-the-curve calculations of metabolite levels obtained from dose-response POMHEX treatment.
    Figure Legend Snippet: POMHEX selectively induces energy stress, inhibits proliferation, and triggers apoptosis in ENO1 -deleted glioma cells. ENO1 -deleted (D423, red), ENO1 -isogenically rescued (D423 ENO1, blue), and ENO1 -WT (LN319, grey) glioma cells were treated with the Enolase inhibitor POMHEX for 72 hours. Cells were harvested for protein lysates and polar metabolites. a . ENO1 -deleted cells experience dose-dependent increase in stress response markers (phosphorylated T346 NDRG1, S73 c-Jun), decrease in proliferation (phosphorylated Histone H3, PLK1), and increase in cell death (cleaved caspsase-3), as indicated by western blot. Such effects are exclusive to ENO1 -deleted cells (left, red) and are absent in ENO1 -WT cells (middle, blue; right, grey). b. Lactate levels were measured by 1 H NMR with the integral of 1.34 ppm doublet normalized to 3-(trimethylsilyl)propionic-2,2,3,3-d4 acid standard and expressed as % of CT [(n=2(CT), mean of n=1 (treated biological replicates)]. A dose-dependent decrease in lactate levels is unique to ENO1 -deleted, but not ENO1 -WT, glioma cells. c. Glycerate levels were used as a marker of Enolase inhibition and were measured by mass spectrometry. Values are expressed as % of CT [(n = 4(CT), mean of n = 2 (treated biological replicates)]. A dose-dependent increase in glycerate levels was observed in ENO1 -deleted but not ENO1 -WT glioma cells. d-e. Phosphocreatine/creatine ratio and pyrophosphate (PPi) levels quantified via mass spectrometry were used as measures of energy stress. The dose-dependent decrease in phosphocreatine to creatine ratio ( d ) and increase in PPi ( e ) in response to POMHEX treatment is specific to ENO1 -deleted glioma cells. Both measurements are expressed as a % of CT [N = 4(CT), mean of N = 2 (treated biological replicates)]. f . Treatment with POMHEX results in depletion of anaplerotic substrates. Top: metabolic map showing relative increases (red) and decreases (blue) of relevant metabolites in glycolysis, hexosamine biosynthesis pathway, non-oxidative pentose phosphate pathway, and TCA cycle in ENO1 -deleted (D423) cells. Bottom: heat map of relevant metabolites in ENO1 -deleted (D423), ENO1 -heterozygous deleted (D502, U343), and ENO1 -WT (LN319) glioma cells. A decrease in TCA metabolites is observed across all cell lines treated with POMHEX, Relative abundance is expressed as area-under-the-curve calculations of metabolite levels obtained from dose-response POMHEX treatment.

    Techniques Used: Western Blot, Nuclear Magnetic Resonance, Marker, Inhibition, Mass Spectrometry

    2) Product Images from "An Enolase Inhibitor for the Targeted Treatment of ENO1-Deleted Cancers"

    Article Title: An Enolase Inhibitor for the Targeted Treatment of ENO1-Deleted Cancers

    Journal: Nature metabolism

    doi: 10.1038/s42255-020-00313-3

    POMHEX selectively induces energy stress, inhibits proliferation, and triggers apoptosis in ENO1 -deleted glioma cells. ENO1 -deleted (D423, red), ENO1 -isogenically rescued (D423 ENO1, blue), and ENO1 -WT (LN319, grey) glioma cells were treated with the Enolase inhibitor POMHEX for 72 hours. Cells were harvested for protein lysates and polar metabolites. a . ENO1 -deleted cells experience dose-dependent increase in stress response markers (phosphorylated T346 NDRG1, S73 c-Jun), decrease in proliferation (phosphorylated Histone H3, PLK1), and increase in cell death (cleaved caspsase-3), as indicated by western blot. Such effects are exclusive to ENO1 -deleted cells (left, red) and are absent in ENO1 -WT cells (middle, blue; right, grey). b. Lactate levels were measured by 1 H NMR with the integral of 1.34 ppm doublet normalized to 3-(trimethylsilyl)propionic-2,2,3,3-d4 acid standard and expressed as % of CT [(n=2(CT), mean of n=1 (treated biological replicates)]. A dose-dependent decrease in lactate levels is unique to ENO1 -deleted, but not ENO1 -WT, glioma cells. c. Glycerate levels were used as a marker of Enolase inhibition and were measured by mass spectrometry. Values are expressed as % of CT [(n = 4(CT), mean of n = 2 (treated biological replicates)]. A dose-dependent increase in glycerate levels was observed in ENO1 -deleted but not ENO1 -WT glioma cells. d-e. Phosphocreatine/creatine ratio and pyrophosphate (PPi) levels quantified via mass spectrometry were used as measures of energy stress. The dose-dependent decrease in phosphocreatine to creatine ratio ( d ) and increase in PPi ( e ) in response to POMHEX treatment is specific to ENO1 -deleted glioma cells. Both measurements are expressed as a % of CT [N = 4(CT), mean of N = 2 (treated biological replicates)]. f . Treatment with POMHEX results in depletion of anaplerotic substrates. Top: metabolic map showing relative increases (red) and decreases (blue) of relevant metabolites in glycolysis, hexosamine biosynthesis pathway, non-oxidative pentose phosphate pathway, and TCA cycle in ENO1 -deleted (D423) cells. Bottom: heat map of relevant metabolites in ENO1 -deleted (D423), ENO1 -heterozygous deleted (D502, U343), and ENO1 -WT (LN319) glioma cells. A decrease in TCA metabolites is observed across all cell lines treated with POMHEX, Relative abundance is expressed as area-under-the-curve calculations of metabolite levels obtained from dose-response POMHEX treatment.
    Figure Legend Snippet: POMHEX selectively induces energy stress, inhibits proliferation, and triggers apoptosis in ENO1 -deleted glioma cells. ENO1 -deleted (D423, red), ENO1 -isogenically rescued (D423 ENO1, blue), and ENO1 -WT (LN319, grey) glioma cells were treated with the Enolase inhibitor POMHEX for 72 hours. Cells were harvested for protein lysates and polar metabolites. a . ENO1 -deleted cells experience dose-dependent increase in stress response markers (phosphorylated T346 NDRG1, S73 c-Jun), decrease in proliferation (phosphorylated Histone H3, PLK1), and increase in cell death (cleaved caspsase-3), as indicated by western blot. Such effects are exclusive to ENO1 -deleted cells (left, red) and are absent in ENO1 -WT cells (middle, blue; right, grey). b. Lactate levels were measured by 1 H NMR with the integral of 1.34 ppm doublet normalized to 3-(trimethylsilyl)propionic-2,2,3,3-d4 acid standard and expressed as % of CT [(n=2(CT), mean of n=1 (treated biological replicates)]. A dose-dependent decrease in lactate levels is unique to ENO1 -deleted, but not ENO1 -WT, glioma cells. c. Glycerate levels were used as a marker of Enolase inhibition and were measured by mass spectrometry. Values are expressed as % of CT [(n = 4(CT), mean of n = 2 (treated biological replicates)]. A dose-dependent increase in glycerate levels was observed in ENO1 -deleted but not ENO1 -WT glioma cells. d-e. Phosphocreatine/creatine ratio and pyrophosphate (PPi) levels quantified via mass spectrometry were used as measures of energy stress. The dose-dependent decrease in phosphocreatine to creatine ratio ( d ) and increase in PPi ( e ) in response to POMHEX treatment is specific to ENO1 -deleted glioma cells. Both measurements are expressed as a % of CT [N = 4(CT), mean of N = 2 (treated biological replicates)]. f . Treatment with POMHEX results in depletion of anaplerotic substrates. Top: metabolic map showing relative increases (red) and decreases (blue) of relevant metabolites in glycolysis, hexosamine biosynthesis pathway, non-oxidative pentose phosphate pathway, and TCA cycle in ENO1 -deleted (D423) cells. Bottom: heat map of relevant metabolites in ENO1 -deleted (D423), ENO1 -heterozygous deleted (D502, U343), and ENO1 -WT (LN319) glioma cells. A decrease in TCA metabolites is observed across all cell lines treated with POMHEX, Relative abundance is expressed as area-under-the-curve calculations of metabolite levels obtained from dose-response POMHEX treatment.

    Techniques Used: Western Blot, Nuclear Magnetic Resonance, Marker, Inhibition, Mass Spectrometry

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    Millipore 3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt
    3 Trimethylsilyl Propionic 2 2 3 3 D4 Acid Sodium Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt/product/Millipore
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    3 trimethylsilyl propionic 2 2 3 3 d4 acid sodium salt - by Bioz Stars, 2022-11
    91/100 stars
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