erk activator c16 paf (MedChemExpress)

MedChemExpress is a verified supplier

MedChemExpress manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

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 66 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c16+paf/C16-PAF/pmc13298773-230-47-50
Average 95 stars, based on 66 article reviews

erk activator c16 paf - by Bioz Stars, 2026-10

95/100 stars

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

Functional Assay:

Article Title: Role of CTGF-LRP1 in impaired healing of cesarean section incisions.
Article Snippet: .. For functional assays, cells were treated for 48 hours with recombinant human CTGF (rhCTGF; HY-P70106, MCE), PD98059 (MEK/ERK inhibitor, HY-12028, MCE), or C16-PAF (MEK/ERK agonist, HY-108635, MCE). .. The human uterine fibroblast (HUF) and rat uterine fibroblast (RUF) were obtained from Procell Biological Technology in China.

Article Title: Role of CTGF-LRP1 in impaired healing of cesarean section incisions
Article Snippet: .. For functional assays, cells were treated for 48 hours with recombinant human CTGF (rhCTGF; HY- P70106 , MCE), PD98059 (MEK/ERK inhibitor, HY-12028, MCE), or C16-PAF (MEK/ERK agonist, HY-108635, MCE). .. The human uterine fibroblast (HUF) and rat uterine fibroblast (RUF) were obtained from Procell Biological Technology in China.

Recombinant:

Transfection:

Article Title: Role of CTGF-LRP1 in impaired healing of cesarean section incisions.
Article Snippet: .. Following transfection with LRP1 siRNA, NC siRNA, lrp1 siRNA or nc siRNA for 48 hours, the cells were subsequently incubated with rhCTGF (HY-P70106, MCE), PD98059 (HY-12028, MCE), or C16-PAF (HY-108635, MCE) for 48 hours. ..

Article Title: Role of CTGF-LRP1 in impaired healing of cesarean section incisions
Article Snippet: .. Following transfection with LRP1 siRNA, NC siRNA, lrp1 siRNA or nc siRNA for 48 hours, the cells were subsequently incubated with rhCTGF (HY- P70106 , MCE), PD98059 (HY-12028, MCE), or C16-PAF (HY-108635, MCE) for 48 hours. ..

Incubation:

Drug discovery:

Article Title: PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury
Article Snippet: .. Endogenous Metabolite Compound Library (HY‐L030), FDA‐Approved Drug Library (HY‐L022), Cl‐amidine hydrochloride (HY‐100574A), VX‐765 (HY‐13205), Z‐DEVD‐FMK (HY‐12466), Necrostatin‐1 (HY‐15760), Sivelestat (HY‐17443), C16 PAF (HY‐108635), LDC7559 (HY‐111674), Rilapladib (HY‐102004), Dapagliflozin (HY‐10450), Empagliflozin (HY‐15409), Canagliflozin (HY‐10451), Ertugliflozin (HY‐15461) and Darapladib (HY‐10521) were obtained from MedChemExpress (Shanghai, China). .. DNase I (D4513), PMA (P1585) and All‐trans retinoic acid (ATRA) (R2625‐50MG) were obtained from Sigma‐Aldrich (Saint Louis, MO, USA). (S)‐Bromoenol Lactone (GC40679) was obtained from GLPBIO (Montclair, NJ, USA).

other:

Article Title: RFRP-3 suppresses ovarian granulosa cell function in Tan sheep via dual signaling pathways: PI3K/AKT/mTOR and MAPK/ERK1/2
Article Snippet: The inhibitory role of RFRP-3 in the hypothalamic-pituitary axis is established, but its direct intra-ovarian actions remain poorly defined.. This study reveals, for the first time, the expression of RFRP-3 and its receptor GPR147 in ovarian granulosa cells of Tan sheep.. We demonstrate that RFRP-3 acts locally to suppress steroidogenesis by downregulating key steroidogenic enzymes (STAR, CYP19A1, HSD17B2).

Review