timp2  (Boster Bio)


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    Boster Bio timp2
    Expression levels of collagen III, matrix <t>metalloproteinase</t> (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P
    Timp2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/timp2/product/Boster Bio
    Average 91 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    timp2 - by Bioz Stars, 2022-12
    91/100 stars

    Images

    1) Product Images from "Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway"

    Article Title: Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2018.3419

    Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P
    Figure Legend Snippet: Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Techniques Used: Expressing, Standard Deviation

    2) Product Images from "Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway"

    Article Title: Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2018.3419

    Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P
    Figure Legend Snippet: Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Techniques Used: Expressing, Standard Deviation

    3) Product Images from "The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway"

    Article Title: The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway

    Journal: Scientific Reports

    doi: 10.1038/srep29975

    Calpastatin induction suppresses PDGF-induced proliferation and migration of VSMCs and collagen I synthesis via inhibition of the MMP2/TGF-β1 pathway mediated by calpain-1/2. ( A ) Cell proliferation was measured by cell counting kit-8 (CCK-8) assays. ( B ) Non-directional cell migration was measured by transwell migration assays. ( C ) Directional migration was measured by scratch wound healing assays. ( D,E ) mRNA levels of collagen I, collagen III, calpain-1, and calpain-2 were determined by qRT-PCR. ( F,I ) Representative images of western blots. ( G,J,K ) Densitometric analyses of calpastatin, calpain-1/2, MMP2, MTIMMP, TIMP2, and TGF-β1. ( H ) Calpain activity was determined by measurement of the fraction of calpain-specific SBDPs, which was calculated by dividing the cleaved spectrin density (145 and 150 kDa) by the total spectrin density (145, 150, and 250 kD). VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; SBDPs, spectrin breakdown products; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; OD, Optical density. Presented values are means ± SEM. N = 6–8/group. * P
    Figure Legend Snippet: Calpastatin induction suppresses PDGF-induced proliferation and migration of VSMCs and collagen I synthesis via inhibition of the MMP2/TGF-β1 pathway mediated by calpain-1/2. ( A ) Cell proliferation was measured by cell counting kit-8 (CCK-8) assays. ( B ) Non-directional cell migration was measured by transwell migration assays. ( C ) Directional migration was measured by scratch wound healing assays. ( D,E ) mRNA levels of collagen I, collagen III, calpain-1, and calpain-2 were determined by qRT-PCR. ( F,I ) Representative images of western blots. ( G,J,K ) Densitometric analyses of calpastatin, calpain-1/2, MMP2, MTIMMP, TIMP2, and TGF-β1. ( H ) Calpain activity was determined by measurement of the fraction of calpain-specific SBDPs, which was calculated by dividing the cleaved spectrin density (145 and 150 kDa) by the total spectrin density (145, 150, and 250 kD). VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; SBDPs, spectrin breakdown products; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; OD, Optical density. Presented values are means ± SEM. N = 6–8/group. * P

    Techniques Used: Migration, Inhibition, Cell Counting, CCK-8 Assay, Quantitative RT-PCR, Western Blot, Activity Assay, Derivative Assay

    Calpastatin overexpression inhibits expression of MMP2/TGF-β1 in carotid restenosis, and MMP2 supplementation reverses the protective effect of calpastatin induction. ( A–C ) Expression of MMP2, MT1MMP, and TIMP2 was determined by immunohistochemical staining in carotid restenosis at 14 days after ligation. Representative images are shown. ( D ) Quantification of MMP2, MT1MMP, and TIMP2 by the IOD/area. ( E,F ) mRNA levels of MMP2/TGF-β1 were determined by qRT-PCR. ( G ) The extent of carotid restenosis was assessed by HE staining. MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; IOD, integral optical density; AdGFP, adenovirus vector encoding green fluorescence protein; AdMMP2, adenovirus vector carrying MMP2 sequence. Presented values are means ± SEM. N = 6–8/group. ** P
    Figure Legend Snippet: Calpastatin overexpression inhibits expression of MMP2/TGF-β1 in carotid restenosis, and MMP2 supplementation reverses the protective effect of calpastatin induction. ( A–C ) Expression of MMP2, MT1MMP, and TIMP2 was determined by immunohistochemical staining in carotid restenosis at 14 days after ligation. Representative images are shown. ( D ) Quantification of MMP2, MT1MMP, and TIMP2 by the IOD/area. ( E,F ) mRNA levels of MMP2/TGF-β1 were determined by qRT-PCR. ( G ) The extent of carotid restenosis was assessed by HE staining. MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; IOD, integral optical density; AdGFP, adenovirus vector encoding green fluorescence protein; AdMMP2, adenovirus vector carrying MMP2 sequence. Presented values are means ± SEM. N = 6–8/group. ** P

    Techniques Used: Over Expression, Expressing, Immunohistochemistry, Staining, Ligation, Quantitative RT-PCR, Plasmid Preparation, Fluorescence, Sequencing

    Schematic diagram depicting the protective effects of calpains inhibition in vascular restenosis by inhibition of MMP2/TGF-β1 signalling. In vascular restenosis, the functional balance of calpastatin and calpains was disturbed, leading to the activation of MMP2/TGF-β1 signalling. It is well known that the MMP2/TGF-β1 pathway is closely related to the proliferation and migration of VSMCs and collagen synthesis. Using TG mice, specific siRNAs against calpain-1/2, AdMMP2, and simvastatin, we revealed that calpastatin induction and calpains inhibition suppress the expression of MMP2/TGF-β1, subsequently preventing the proliferation and migration of VSMCs and collagen synthesis, finally attenuating vascular restenosis. Most importantly, calpain-1 is the major molecule in the development of vascular restenosis by influencing all aspects. In contrast, calpain-2 only played an auxiliary role in restenosis processes by enhancing VSMC migration. Moreover, simvastatin may inhibit the expression of calpain-1/2 by accelerating HIF-1α degradation to attenuate vascular restenosis. TG, calpastatin transgene; VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1. TG, calpastatin transgene; siRNA, small interfering RNA; AdMMP2, adenoviral vector carrying MMP2 ; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1.
    Figure Legend Snippet: Schematic diagram depicting the protective effects of calpains inhibition in vascular restenosis by inhibition of MMP2/TGF-β1 signalling. In vascular restenosis, the functional balance of calpastatin and calpains was disturbed, leading to the activation of MMP2/TGF-β1 signalling. It is well known that the MMP2/TGF-β1 pathway is closely related to the proliferation and migration of VSMCs and collagen synthesis. Using TG mice, specific siRNAs against calpain-1/2, AdMMP2, and simvastatin, we revealed that calpastatin induction and calpains inhibition suppress the expression of MMP2/TGF-β1, subsequently preventing the proliferation and migration of VSMCs and collagen synthesis, finally attenuating vascular restenosis. Most importantly, calpain-1 is the major molecule in the development of vascular restenosis by influencing all aspects. In contrast, calpain-2 only played an auxiliary role in restenosis processes by enhancing VSMC migration. Moreover, simvastatin may inhibit the expression of calpain-1/2 by accelerating HIF-1α degradation to attenuate vascular restenosis. TG, calpastatin transgene; VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1. TG, calpastatin transgene; siRNA, small interfering RNA; AdMMP2, adenoviral vector carrying MMP2 ; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1.

    Techniques Used: Inhibition, Functional Assay, Activation Assay, Migration, Mouse Assay, Expressing, Derivative Assay, Small Interfering RNA, Plasmid Preparation

    4) Product Images from "The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway"

    Article Title: The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway

    Journal: Scientific Reports

    doi: 10.1038/srep29975

    Calpastatin induction suppresses PDGF-induced proliferation and migration of VSMCs and collagen I synthesis via inhibition of the MMP2/TGF-β1 pathway mediated by calpain-1/2. ( A ) Cell proliferation was measured by cell counting kit-8 (CCK-8) assays. ( B ) Non-directional cell migration was measured by transwell migration assays. ( C ) Directional migration was measured by scratch wound healing assays. ( D,E ) mRNA levels of collagen I, collagen III, calpain-1, and calpain-2 were determined by qRT-PCR. ( F,I ) Representative images of western blots. ( G,J,K ) Densitometric analyses of calpastatin, calpain-1/2, MMP2, MTIMMP, TIMP2, and TGF-β1. ( H ) Calpain activity was determined by measurement of the fraction of calpain-specific SBDPs, which was calculated by dividing the cleaved spectrin density (145 and 150 kDa) by the total spectrin density (145, 150, and 250 kD). VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; SBDPs, spectrin breakdown products; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; OD, Optical density. Presented values are means ± SEM. N = 6–8/group. * P
    Figure Legend Snippet: Calpastatin induction suppresses PDGF-induced proliferation and migration of VSMCs and collagen I synthesis via inhibition of the MMP2/TGF-β1 pathway mediated by calpain-1/2. ( A ) Cell proliferation was measured by cell counting kit-8 (CCK-8) assays. ( B ) Non-directional cell migration was measured by transwell migration assays. ( C ) Directional migration was measured by scratch wound healing assays. ( D,E ) mRNA levels of collagen I, collagen III, calpain-1, and calpain-2 were determined by qRT-PCR. ( F,I ) Representative images of western blots. ( G,J,K ) Densitometric analyses of calpastatin, calpain-1/2, MMP2, MTIMMP, TIMP2, and TGF-β1. ( H ) Calpain activity was determined by measurement of the fraction of calpain-specific SBDPs, which was calculated by dividing the cleaved spectrin density (145 and 150 kDa) by the total spectrin density (145, 150, and 250 kD). VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; SBDPs, spectrin breakdown products; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; OD, Optical density. Presented values are means ± SEM. N = 6–8/group. * P

    Techniques Used: Migration, Inhibition, Cell Counting, CCK-8 Assay, Quantitative RT-PCR, Western Blot, Activity Assay, Derivative Assay

    Calpastatin overexpression inhibits expression of MMP2/TGF-β1 in carotid restenosis, and MMP2 supplementation reverses the protective effect of calpastatin induction. ( A–C ) Expression of MMP2, MT1MMP, and TIMP2 was determined by immunohistochemical staining in carotid restenosis at 14 days after ligation. Representative images are shown. ( D ) Quantification of MMP2, MT1MMP, and TIMP2 by the IOD/area. ( E,F ) mRNA levels of MMP2/TGF-β1 were determined by qRT-PCR. ( G ) The extent of carotid restenosis was assessed by HE staining. MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; IOD, integral optical density; AdGFP, adenovirus vector encoding green fluorescence protein; AdMMP2, adenovirus vector carrying MMP2 sequence. Presented values are means ± SEM. N = 6–8/group. ** P
    Figure Legend Snippet: Calpastatin overexpression inhibits expression of MMP2/TGF-β1 in carotid restenosis, and MMP2 supplementation reverses the protective effect of calpastatin induction. ( A–C ) Expression of MMP2, MT1MMP, and TIMP2 was determined by immunohistochemical staining in carotid restenosis at 14 days after ligation. Representative images are shown. ( D ) Quantification of MMP2, MT1MMP, and TIMP2 by the IOD/area. ( E,F ) mRNA levels of MMP2/TGF-β1 were determined by qRT-PCR. ( G ) The extent of carotid restenosis was assessed by HE staining. MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β 1, transforming growth factor-β 1; IOD, integral optical density; AdGFP, adenovirus vector encoding green fluorescence protein; AdMMP2, adenovirus vector carrying MMP2 sequence. Presented values are means ± SEM. N = 6–8/group. ** P

    Techniques Used: Over Expression, Expressing, Immunohistochemistry, Staining, Ligation, Quantitative RT-PCR, Plasmid Preparation, Fluorescence, Sequencing

    Schematic diagram depicting the protective effects of calpains inhibition in vascular restenosis by inhibition of MMP2/TGF-β1 signalling. In vascular restenosis, the functional balance of calpastatin and calpains was disturbed, leading to the activation of MMP2/TGF-β1 signalling. It is well known that the MMP2/TGF-β1 pathway is closely related to the proliferation and migration of VSMCs and collagen synthesis. Using TG mice, specific siRNAs against calpain-1/2, AdMMP2, and simvastatin, we revealed that calpastatin induction and calpains inhibition suppress the expression of MMP2/TGF-β1, subsequently preventing the proliferation and migration of VSMCs and collagen synthesis, finally attenuating vascular restenosis. Most importantly, calpain-1 is the major molecule in the development of vascular restenosis by influencing all aspects. In contrast, calpain-2 only played an auxiliary role in restenosis processes by enhancing VSMC migration. Moreover, simvastatin may inhibit the expression of calpain-1/2 by accelerating HIF-1α degradation to attenuate vascular restenosis. TG, calpastatin transgene; VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1. TG, calpastatin transgene; siRNA, small interfering RNA; AdMMP2, adenoviral vector carrying MMP2 ; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1.
    Figure Legend Snippet: Schematic diagram depicting the protective effects of calpains inhibition in vascular restenosis by inhibition of MMP2/TGF-β1 signalling. In vascular restenosis, the functional balance of calpastatin and calpains was disturbed, leading to the activation of MMP2/TGF-β1 signalling. It is well known that the MMP2/TGF-β1 pathway is closely related to the proliferation and migration of VSMCs and collagen synthesis. Using TG mice, specific siRNAs against calpain-1/2, AdMMP2, and simvastatin, we revealed that calpastatin induction and calpains inhibition suppress the expression of MMP2/TGF-β1, subsequently preventing the proliferation and migration of VSMCs and collagen synthesis, finally attenuating vascular restenosis. Most importantly, calpain-1 is the major molecule in the development of vascular restenosis by influencing all aspects. In contrast, calpain-2 only played an auxiliary role in restenosis processes by enhancing VSMC migration. Moreover, simvastatin may inhibit the expression of calpain-1/2 by accelerating HIF-1α degradation to attenuate vascular restenosis. TG, calpastatin transgene; VSMCs, vascular smooth muscle cells; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1. TG, calpastatin transgene; siRNA, small interfering RNA; AdMMP2, adenoviral vector carrying MMP2 ; PDGF, platelet-derived growth factor; MMP2, matrix metalloproteinase 2; MT1MMP, membrane-type matrix metalloproteinase-1; TIMP2, tissue inhibitor of matrix metalloproteinase-2; TGF-β1, transforming growth factor-β1.

    Techniques Used: Inhibition, Functional Assay, Activation Assay, Migration, Mouse Assay, Expressing, Derivative Assay, Small Interfering RNA, Plasmid Preparation

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    Boster Bio timp2
    Expression levels of collagen III, matrix <t>metalloproteinase</t> (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P
    Timp2, supplied by Boster Bio, 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/timp2/product/Boster Bio
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    timp2 - by Bioz Stars, 2022-12
    91/100 stars
      Buy from Supplier

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    Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Journal: International Journal of Molecular Medicine

    Article Title: Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway

    doi: 10.3892/ijmm.2018.3419

    Figure Lengend Snippet: Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Article Snippet: Rabbit polyclonal anti-JAK-1 (cat. no. A00330), rabbit polyclonal anti-JAK-2 (cat. no. BA3398), rabbit polyclonal anti-collagen III (cat. no. BA0326), rabbit polyclonal anti-transforming growth factor (TGF)-β (cat. no. BA0290), rabbit polyclonal antitumor necrosis factor (TNF)-α (cat. no. BA14903), rabbit polyclonal anti-nuclear factor (NF)-κB (cat. no. BM3946), mouse anti-STAT1 (cat. no. BA0619-2), mouse anti-STAT3 (cat. no. BA0621), mouse anti-STAT5 (cat. no. BA1411), mouse anti-STAT6 (cat. no. BA1414), mouse anti-cystathionine-γ-lyase (CSE; cat. no. BA3605), mouse anti-tissue inhibitor of metalloproteinase (TIMP)2 (cat. no. BA0576), mouse anti-matrix metalloproteinase (MMP)8 (cat. no. BA2201), mouse anti-MMP14 (cat. no. BA1278) and rabbit polyclonal anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; cat. no. BM3874), were all purchased from Wuhan Boster Biological Technology, Ltd. (Wuhan, China).

    Techniques: Expressing, Standard Deviation

    Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Journal: International Journal of Molecular Medicine

    Article Title: Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway

    doi: 10.3892/ijmm.2018.3419

    Figure Lengend Snippet: Expression levels of collagen III, matrix metalloproteinase (MMP)8, MMP14 and tissue inhibitor of metalloproteinase (TIMP)2 in each group. Data are expressed as mean ± standard deviation (n=3). * P

    Article Snippet: Rabbit polyclonal anti-JAK-1 (cat. no. A00330), rabbit polyclonal anti-JAK-2 (cat. no. BA3398), rabbit polyclonal anti-collagen III (cat. no. BA0326), rabbit polyclonal anti-transforming growth factor (TGF)-β (cat. no. BA0290), rabbit polyclonal antitumor necrosis factor (TNF)-α (cat. no. BA14903), rabbit polyclonal anti-nuclear factor (NF)-κB (cat. no. BM3946), mouse anti-STAT1 (cat. no. BA0619-2), mouse anti-STAT3 (cat. no. BA0621), mouse anti-STAT5 (cat. no. BA1411), mouse anti-STAT6 (cat. no. BA1414), mouse anti-cystathionine-γ-lyase (CSE; cat. no. BA3605), mouse anti-tissue inhibitor of metalloproteinase (TIMP)2 (cat. no. BA0576), mouse anti-matrix metalloproteinase (MMP)8 (cat. no. BA2201), mouse anti-MMP14 (cat. no. BA1278) and rabbit polyclonal anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; cat. no. BM3874), were all purchased from Wuhan Boster Biological Technology, Ltd. (Wuhan, China).

    Techniques: Expressing, Standard Deviation