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erk activator c16 paf  (MedChemExpress)


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    MedChemExpress erk activator c16 paf
    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator <t>(C16-PAF,</t> ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .
    Erk Activator C16 Paf, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/paf/C16-PAF/pmc13298773-230-47-50
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    erk activator c16 paf - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Angptl5 restricts primitive hematopoiesis by promoting retinoic acid signaling in zebrafish"

    Article Title: Angptl5 restricts primitive hematopoiesis by promoting retinoic acid signaling in zebrafish

    Journal: PLOS Biology

    doi: 10.1371/journal.pbio.3003858

    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator (C16-PAF, ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .
    Figure Legend Snippet: (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator (C16-PAF, ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .

    Techniques Used: Injection, Control, ChIP-qPCR, Binding Assay, Chromatin Immunoprecipitation



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    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator <t>(C16-PAF,</t> ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .
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    Novus Biologicals mouse paf ah pla2g7 lp pla2 elisa kit
    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator <t>(C16-PAF,</t> ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .
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    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator <t>(C16-PAF,</t> ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .
    Mouse Pla2g7 Paf Ah Lp Pla2 Elisa Kit Novus Biologicals Nbp2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator (C16-PAF, ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .

    Journal: PLOS Biology

    Article Title: Angptl5 restricts primitive hematopoiesis by promoting retinoic acid signaling in zebrafish

    doi: 10.1371/journal.pbio.3003858

    Figure Lengend Snippet: (A) WISH of cyp26a1 in WT embryos. Embryos were treated with ERK activator (C16-PAF, ERKa) or ERK inhibitor (Mirdametinib, ERKi) from the shield stage, or injected with angptl5 + itga6l + itgb5 mRNA at the 1-cell stage. Untreated embryos were used as control. (B–D) Schematic diagram of experimental setup (B) for WISH of dhrs9 and aldh1a2 in WT embryos. caERK2 (C) or angptl5 + itga6l + itgb5 (D) mRNA injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (E–G) Schematic diagram of experimental setup (E) for WISH of dhrs9 . WT embryos were first injected with angptl5 mRNA at the 1-cell stage. Subsequently, itga6l ± itgb5 mRNA was injected into one blastomere on the animal pole at the 128-cell stage. Embryos were then continuously treated with or without ERK inhibitor until the shield stage (G) . Uninjected embryos and only angptl5 mRNA injected embryos (F) were used as control. (H) WISH of dhrs9 in WT embryos. caERK2 mRNA ± junba/bb MO injected into one blastomere on the animal pole at the 128-cell stage and then detected at 6 hpf. (I) ChIP-qPCR analysis of Junb binding to upstream regions of dhrs9. Embryos injected with HA-Junba mRNA were subjected to chromatin immunoprecipitation with HA-agarose, using IgG-agarose as a control. Enrichment at three predicted binding sites upstream of the dhrs9 gene was quantified by qPCR. Data are presented as the mean ± SD from three independent biological replicates. *** P < 0.001 (Unpaired t t est). (J and K) WISH of spi1b in angptl5 Δ10/Δ10 embryos. Embryos were injected with itga6l + itgb5 mRNA at the 1-cell stage and treated with or without ERK inhibitor from the shield stage to the 18-somite stage (J), or injected with caERK 2 mRNA at the 1-cell stage and treated with or without RA receptor antagonist AGN 193109 (K). Uninjected embryos were used as control. Statistics are shown below. Data presented as the mean ± SD, n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + itga6l + itgb5 ) = 26, n( angptl5 Δ10/Δ10 + itga6l + itgb5 + ERKi) = 28 (J); n( angptl5 Δ10/Δ10 ) = 22, n( angptl5 Δ10/Δ10 + caERK ) = 22, and n( angptl5 Δ10/Δ10 + caERKi + AGN) = 26 (K). Statistical significance: ** P < 0.01, *** P < 0.001 (One-way ANOVA). LV, lateral view; AV, animal view (C–H), anterior view (J and K). The data for this figure can be found in .

    Article Snippet: Detailed pharmacological parameters and experimental concentrations are tabulated below: RA (sigma), Aldehyde dehydrogenase inhibitors 4-diethylaminobenzaldehyde (DEAB) (MCE, 10 μM), RA receptor (RARs) antagonists AGN 193109 (MCE, 20 μM), FAK inhibitor Defactinib (MCE, 2 μM/8 μM), MAPK inhibitor Adezmapimod (MCE, 10 μM), ERK inhibitor Mirdametinib (MCE, 10 μM), ERK activator C16-PAF (MCE, 1 μM/5 μM), NF-κB inhibitor BAY 11-7082 (MCE, 0.1 μg/mL, 0.4 μg/mL).

    Techniques: Injection, Control, ChIP-qPCR, Binding Assay, Chromatin Immunoprecipitation