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akt cat no 66444 1 ig  (Proteintech)


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    Structured Review

    Proteintech akt cat no 66444 1 ig
    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
    Akt Cat No 66444 1 Ig, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1775 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/akt cat no 66444 1 ig/product/Proteintech
    Average 96 stars, based on 1775 article reviews
    akt cat no 66444 1 ig - by Bioz Stars, 2026-02
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    1) Product Images from "Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway"

    Article Title: Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway

    Journal: Biomedical Reports

    doi: 10.3892/br.2025.2092

    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
    Figure Legend Snippet: Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Techniques Used: Immunoprecipitation, Expressing, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, Negative Control, Small Interfering RNA

    Silencing of ALOX15 mitigates acute coronary syndrome progression in vitro through the FGFR2/PI3K/AKT signaling pathway. (A) The expression of FGFR2 in HCAECs after transfection with OE-FGFR2 or OE-NC was detected by RT-qPCR. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs following different treatments was detected by RT-qPCR. (C) The protein levels of FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs following various treatments were determined by western blotting. (D, E) The migration of HCAECs following different treatments was assessed by scratch wound healing assays. Scale bar, 100 µm. (F) The viability of HCAECs following various treatments was measured by Cell Counting Kit-8 assays. * P<0.05, ** P<0.01 and *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
    Figure Legend Snippet: Silencing of ALOX15 mitigates acute coronary syndrome progression in vitro through the FGFR2/PI3K/AKT signaling pathway. (A) The expression of FGFR2 in HCAECs after transfection with OE-FGFR2 or OE-NC was detected by RT-qPCR. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs following different treatments was detected by RT-qPCR. (C) The protein levels of FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs following various treatments were determined by western blotting. (D, E) The migration of HCAECs following different treatments was assessed by scratch wound healing assays. Scale bar, 100 µm. (F) The viability of HCAECs following various treatments was measured by Cell Counting Kit-8 assays. * P<0.05, ** P<0.01 and *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Techniques Used: In Vitro, Expressing, Transfection, Quantitative RT-PCR, Western Blot, Migration, Cell Counting, Over Expression, Negative Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Small Interfering RNA

    ALOX15 silencing suppresses the activation of the FGFR2/PI3K/AKT signaling pathway. The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in rats with ACS after injection of shRNA ALOX15 or shRNA NC were determined by western blotting. *** P<0.001 vs. sham; ### P<0.001 vs. ACS model + shRNA NC. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; p-, phosphorylated; ACS, acute coronary syndrome; shRNA, short hairpin RNA; NC, negative control; NS, no significance.
    Figure Legend Snippet: ALOX15 silencing suppresses the activation of the FGFR2/PI3K/AKT signaling pathway. The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in rats with ACS after injection of shRNA ALOX15 or shRNA NC were determined by western blotting. *** P<0.001 vs. sham; ### P<0.001 vs. ACS model + shRNA NC. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; p-, phosphorylated; ACS, acute coronary syndrome; shRNA, short hairpin RNA; NC, negative control; NS, no significance.

    Techniques Used: Activation Assay, Injection, shRNA, Western Blot, Negative Control



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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and <t>p-AKT</t> in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.
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    Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Journal: Biomedical Reports

    Article Title: Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway

    doi: 10.3892/br.2025.2092

    Figure Lengend Snippet: Effects of ALOX15 on the FGFR2/PI3K/AKT signaling pathway in HCAECs. (A) Co-immunoprecipitation assays of ALOX15 and FGFR2 in HCAECs. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC was detected by reverse transcription-quantitative PCR. *** P<0.001. (C) The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs after transfection with OE-ALOX15/OE-NC or siRNA ALOX15/siRNA NC were determined by western blotting. *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Article Snippet: TRIzol reagent (cat. no. 10606ES60), Hifair ® II 1st Strand cDNA Synthesis SuperMix (cat. no. 11123ES60) and Hieff ® qPCR SYBR Green Master Mix (cat. no. 11202ES08) were procured from Shanghai Yeasen Biotechnology Co., Ltd. Primary antibodies AKT (cat. no. 60203-2-Ig), phoshorylated (p)-AKT (cat. no. 66444-1-Ig), GAPDH (cat. no. 60004-1-Ig) and HRP-conjugated secondary antibodies (cat. no. SA00001-2) were obtained from Proteintech Group, Inc. Primary antibodies p-PI3K (cat. no. 4228T) and FGFR2 (cat. no. 23328) were purchased from Cell Signaling Technology, Inc., and PI3K antibody (cat. no. ab191606) was sourced from Abcam.

    Techniques: Immunoprecipitation, Expressing, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, Negative Control, Small Interfering RNA

    Silencing of ALOX15 mitigates acute coronary syndrome progression in vitro through the FGFR2/PI3K/AKT signaling pathway. (A) The expression of FGFR2 in HCAECs after transfection with OE-FGFR2 or OE-NC was detected by RT-qPCR. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs following different treatments was detected by RT-qPCR. (C) The protein levels of FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs following various treatments were determined by western blotting. (D, E) The migration of HCAECs following different treatments was assessed by scratch wound healing assays. Scale bar, 100 µm. (F) The viability of HCAECs following various treatments was measured by Cell Counting Kit-8 assays. * P<0.05, ** P<0.01 and *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Journal: Biomedical Reports

    Article Title: Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway

    doi: 10.3892/br.2025.2092

    Figure Lengend Snippet: Silencing of ALOX15 mitigates acute coronary syndrome progression in vitro through the FGFR2/PI3K/AKT signaling pathway. (A) The expression of FGFR2 in HCAECs after transfection with OE-FGFR2 or OE-NC was detected by RT-qPCR. (B) The mRNA expression of ALOX15 and FGFR2 in HCAECs following different treatments was detected by RT-qPCR. (C) The protein levels of FGFR2, PI3K, p-PI3K, AKT and p-AKT in HCAECs following various treatments were determined by western blotting. (D, E) The migration of HCAECs following different treatments was assessed by scratch wound healing assays. Scale bar, 100 µm. (F) The viability of HCAECs following various treatments was measured by Cell Counting Kit-8 assays. * P<0.05, ** P<0.01 and *** P<0.001. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; HCAECs, human primary coronary artery endothelial cells; OE, overexpression; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; siRNA, small interfering RNA; p-, phosphorylated; NS, not significant.

    Article Snippet: TRIzol reagent (cat. no. 10606ES60), Hifair ® II 1st Strand cDNA Synthesis SuperMix (cat. no. 11123ES60) and Hieff ® qPCR SYBR Green Master Mix (cat. no. 11202ES08) were procured from Shanghai Yeasen Biotechnology Co., Ltd. Primary antibodies AKT (cat. no. 60203-2-Ig), phoshorylated (p)-AKT (cat. no. 66444-1-Ig), GAPDH (cat. no. 60004-1-Ig) and HRP-conjugated secondary antibodies (cat. no. SA00001-2) were obtained from Proteintech Group, Inc. Primary antibodies p-PI3K (cat. no. 4228T) and FGFR2 (cat. no. 23328) were purchased from Cell Signaling Technology, Inc., and PI3K antibody (cat. no. ab191606) was sourced from Abcam.

    Techniques: In Vitro, Expressing, Transfection, Quantitative RT-PCR, Western Blot, Migration, Cell Counting, Over Expression, Negative Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Small Interfering RNA

    ALOX15 silencing suppresses the activation of the FGFR2/PI3K/AKT signaling pathway. The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in rats with ACS after injection of shRNA ALOX15 or shRNA NC were determined by western blotting. *** P<0.001 vs. sham; ### P<0.001 vs. ACS model + shRNA NC. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; p-, phosphorylated; ACS, acute coronary syndrome; shRNA, short hairpin RNA; NC, negative control; NS, no significance.

    Journal: Biomedical Reports

    Article Title: Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway

    doi: 10.3892/br.2025.2092

    Figure Lengend Snippet: ALOX15 silencing suppresses the activation of the FGFR2/PI3K/AKT signaling pathway. The protein levels of ALOX15, FGFR2, PI3K, p-PI3K, AKT and p-AKT in rats with ACS after injection of shRNA ALOX15 or shRNA NC were determined by western blotting. *** P<0.001 vs. sham; ### P<0.001 vs. ACS model + shRNA NC. ALOX15, 12/15-lipoxygenase; FGFR2, fibroblast growth factor receptor 2; p-, phosphorylated; ACS, acute coronary syndrome; shRNA, short hairpin RNA; NC, negative control; NS, no significance.

    Article Snippet: TRIzol reagent (cat. no. 10606ES60), Hifair ® II 1st Strand cDNA Synthesis SuperMix (cat. no. 11123ES60) and Hieff ® qPCR SYBR Green Master Mix (cat. no. 11202ES08) were procured from Shanghai Yeasen Biotechnology Co., Ltd. Primary antibodies AKT (cat. no. 60203-2-Ig), phoshorylated (p)-AKT (cat. no. 66444-1-Ig), GAPDH (cat. no. 60004-1-Ig) and HRP-conjugated secondary antibodies (cat. no. SA00001-2) were obtained from Proteintech Group, Inc. Primary antibodies p-PI3K (cat. no. 4228T) and FGFR2 (cat. no. 23328) were purchased from Cell Signaling Technology, Inc., and PI3K antibody (cat. no. ab191606) was sourced from Abcam.

    Techniques: Activation Assay, Injection, shRNA, Western Blot, Negative Control