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  • 91
    Sino Biological elisa kit
    EGFR levels confirmed by western blot analysis and <t>ELISA</t> in <t>CAD</t> patients and control subjects. (A) Western blotting images of plasma EGFR and loading control GAPDH were assayed in CAD patients and controls. (B) Quantification of relative intensity levels of EGFR in CAD patients and controls adjusted for loading control. ImageJ software was used. (C) ELISA-based comparison of mean EGFR levels between the CAD patients and control groups. A significantly higher level of EGFR was observed in the MI and SA groups in comparison with controls. (D) EGFR levels were only significantly different between male MI groups in comparison with male control group. The EGFR levels were significantly different between female MI and SA groups when compared with controls. *P≤0.05, **P≤0.001. EGFR, epidermal growth factor receptor; CAD, coronary artery disease; MI, myocardial infarction; SA, stable angina.
    Elisa Kit, supplied by Sino Biological, 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/elisa kit/product/Sino Biological
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    94
    R&D Systems human trem 2 antibody
    EGFR levels confirmed by western blot analysis and <t>ELISA</t> in <t>CAD</t> patients and control subjects. (A) Western blotting images of plasma EGFR and loading control GAPDH were assayed in CAD patients and controls. (B) Quantification of relative intensity levels of EGFR in CAD patients and controls adjusted for loading control. ImageJ software was used. (C) ELISA-based comparison of mean EGFR levels between the CAD patients and control groups. A significantly higher level of EGFR was observed in the MI and SA groups in comparison with controls. (D) EGFR levels were only significantly different between male MI groups in comparison with male control group. The EGFR levels were significantly different between female MI and SA groups when compared with controls. *P≤0.05, **P≤0.001. EGFR, epidermal growth factor receptor; CAD, coronary artery disease; MI, myocardial infarction; SA, stable angina.
    Human Trem 2 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human trem 2 antibody/product/R&D Systems
    Average 94 stars, based on 1 article reviews
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    93
    Sino Biological trem 2 matched elisa antibody pair set human
    EGFR levels confirmed by western blot analysis and <t>ELISA</t> in <t>CAD</t> patients and control subjects. (A) Western blotting images of plasma EGFR and loading control GAPDH were assayed in CAD patients and controls. (B) Quantification of relative intensity levels of EGFR in CAD patients and controls adjusted for loading control. ImageJ software was used. (C) ELISA-based comparison of mean EGFR levels between the CAD patients and control groups. A significantly higher level of EGFR was observed in the MI and SA groups in comparison with controls. (D) EGFR levels were only significantly different between male MI groups in comparison with male control group. The EGFR levels were significantly different between female MI and SA groups when compared with controls. *P≤0.05, **P≤0.001. EGFR, epidermal growth factor receptor; CAD, coronary artery disease; MI, myocardial infarction; SA, stable angina.
    Trem 2 Matched Elisa Antibody Pair Set Human, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trem 2 matched elisa antibody pair set human/product/Sino Biological
    Average 93 stars, based on 1 article reviews
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    99
    Cell Signaling Technology Inc erk1 2
    Schematic representation of the canonical Wnt signaling function in regulation of cardiac metabolism under the sedentary conditions ( A ) and after the endurance training ( B ). ( A ) Heterozygous knockout of β-catenin inhibits canonical Wnt signaling and downregulates β-catenin target genes ( c-Myc , c-Fos ). This leads to decreased cardiomyocytes size. The higher levels of ANP and β-MHC may lead to the lower heart rate. Canonical Wnt signaling is involved in FA metabolism and regulation of mitochondria function via its targets c-Myc and PDK1. Decreased canonical Wnt signaling is associated with the activation of Pi3K–Akt and <t>MAPK/Erk1/2</t> signaling pathways. Altogether, this causes the inhibition of lipolysis and the activation of glucose uptake in hearts of WT/CKO mice. Activation of β-oxidation and glucose oxidation along with lower activity of complex I lead to the accumulation of NADH, which promotes mitochondrial dysfunction. ( B ) The lower level of canonical Wnt signaling attenuates the cardiomyocytes hypertrophy. Adaptation of WT/CKO mice to the endurance training is accompanied by activation of AMPK and a stronger activation of pre-activated Pi3K–AKT and MAPK/Erk1/2 signaling pathways. Increased AMPK leads to the inhibition of lipolysis and activation of β-oxidation. Activation of AMPK, Pi3K–AKT, and MAPK/Erk1/2 signaling pathways stimulates FA and glucose uptake. Downregulation of canonical Wnt signaling reduces mitochondria biogenesis and OXPHOS activity in the heart during adaptation to the endurance training. Decreased OXPHOS protein level and activity along with enhanced β-oxidation further exacerbate mitochondrial dysfunction. Notes: Red—observed increase; blue—observed decrease; orange—possible increase; green—possible decrease; black—remain unchanged relative to relevant WT/WT mice.
    Erk1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk1 2/product/Cell Signaling Technology Inc
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    Image Search Results


    EGFR levels confirmed by western blot analysis and ELISA in CAD patients and control subjects. (A) Western blotting images of plasma EGFR and loading control GAPDH were assayed in CAD patients and controls. (B) Quantification of relative intensity levels of EGFR in CAD patients and controls adjusted for loading control. ImageJ software was used. (C) ELISA-based comparison of mean EGFR levels between the CAD patients and control groups. A significantly higher level of EGFR was observed in the MI and SA groups in comparison with controls. (D) EGFR levels were only significantly different between male MI groups in comparison with male control group. The EGFR levels were significantly different between female MI and SA groups when compared with controls. *P≤0.05, **P≤0.001. EGFR, epidermal growth factor receptor; CAD, coronary artery disease; MI, myocardial infarction; SA, stable angina.

    Journal: Molecular Medicine Reports

    Article Title: Integrative gene ontology and network analysis of coronary artery disease associated genes suggests potential role of ErbB pathway gene EGFR

    doi: 10.3892/mmr.2018.8393

    Figure Lengend Snippet: EGFR levels confirmed by western blot analysis and ELISA in CAD patients and control subjects. (A) Western blotting images of plasma EGFR and loading control GAPDH were assayed in CAD patients and controls. (B) Quantification of relative intensity levels of EGFR in CAD patients and controls adjusted for loading control. ImageJ software was used. (C) ELISA-based comparison of mean EGFR levels between the CAD patients and control groups. A significantly higher level of EGFR was observed in the MI and SA groups in comparison with controls. (D) EGFR levels were only significantly different between male MI groups in comparison with male control group. The EGFR levels were significantly different between female MI and SA groups when compared with controls. *P≤0.05, **P≤0.001. EGFR, epidermal growth factor receptor; CAD, coronary artery disease; MI, myocardial infarction; SA, stable angina.

    Article Snippet: The plasma level of EGFR was quantified in 342 CAD patients and 342 control samples using an ELISA kit (cat. no. SEK10001; Sino Biological Inc., Beijing, China).

    Techniques: Western Blot, Enzyme-linked Immunosorbent Assay, Software

    An overview of the biomarker prioritization method. The method of biomarker prioritization involves the following: Step 1, selection of CAD related genes from CADgene database; Step 2, gene filtration based on GO and DO; Step 3, the gene set obtained was used for network construction, analysis, identification of hub and pathway enrichment analysis; and, Step 4, biological validation using WB, ELISA and statistical assessment of the biomarker. GO, gene ontology; DO, disease ontology; WB, western blot analysis; CAD, coronary artery disease; EGFR, epidermal growth factor receptor.

    Journal: Molecular Medicine Reports

    Article Title: Integrative gene ontology and network analysis of coronary artery disease associated genes suggests potential role of ErbB pathway gene EGFR

    doi: 10.3892/mmr.2018.8393

    Figure Lengend Snippet: An overview of the biomarker prioritization method. The method of biomarker prioritization involves the following: Step 1, selection of CAD related genes from CADgene database; Step 2, gene filtration based on GO and DO; Step 3, the gene set obtained was used for network construction, analysis, identification of hub and pathway enrichment analysis; and, Step 4, biological validation using WB, ELISA and statistical assessment of the biomarker. GO, gene ontology; DO, disease ontology; WB, western blot analysis; CAD, coronary artery disease; EGFR, epidermal growth factor receptor.

    Article Snippet: The plasma level of EGFR was quantified in 342 CAD patients and 342 control samples using an ELISA kit (cat. no. SEK10001; Sino Biological Inc., Beijing, China).

    Techniques: Biomarker Assay, Selection, Filtration, Western Blot, Enzyme-linked Immunosorbent Assay

    Schematic representation of the canonical Wnt signaling function in regulation of cardiac metabolism under the sedentary conditions ( A ) and after the endurance training ( B ). ( A ) Heterozygous knockout of β-catenin inhibits canonical Wnt signaling and downregulates β-catenin target genes ( c-Myc , c-Fos ). This leads to decreased cardiomyocytes size. The higher levels of ANP and β-MHC may lead to the lower heart rate. Canonical Wnt signaling is involved in FA metabolism and regulation of mitochondria function via its targets c-Myc and PDK1. Decreased canonical Wnt signaling is associated with the activation of Pi3K–Akt and MAPK/Erk1/2 signaling pathways. Altogether, this causes the inhibition of lipolysis and the activation of glucose uptake in hearts of WT/CKO mice. Activation of β-oxidation and glucose oxidation along with lower activity of complex I lead to the accumulation of NADH, which promotes mitochondrial dysfunction. ( B ) The lower level of canonical Wnt signaling attenuates the cardiomyocytes hypertrophy. Adaptation of WT/CKO mice to the endurance training is accompanied by activation of AMPK and a stronger activation of pre-activated Pi3K–AKT and MAPK/Erk1/2 signaling pathways. Increased AMPK leads to the inhibition of lipolysis and activation of β-oxidation. Activation of AMPK, Pi3K–AKT, and MAPK/Erk1/2 signaling pathways stimulates FA and glucose uptake. Downregulation of canonical Wnt signaling reduces mitochondria biogenesis and OXPHOS activity in the heart during adaptation to the endurance training. Decreased OXPHOS protein level and activity along with enhanced β-oxidation further exacerbate mitochondrial dysfunction. Notes: Red—observed increase; blue—observed decrease; orange—possible increase; green—possible decrease; black—remain unchanged relative to relevant WT/WT mice.

    Journal: Life

    Article Title: β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice

    doi: 10.3390/life10120357

    Figure Lengend Snippet: Schematic representation of the canonical Wnt signaling function in regulation of cardiac metabolism under the sedentary conditions ( A ) and after the endurance training ( B ). ( A ) Heterozygous knockout of β-catenin inhibits canonical Wnt signaling and downregulates β-catenin target genes ( c-Myc , c-Fos ). This leads to decreased cardiomyocytes size. The higher levels of ANP and β-MHC may lead to the lower heart rate. Canonical Wnt signaling is involved in FA metabolism and regulation of mitochondria function via its targets c-Myc and PDK1. Decreased canonical Wnt signaling is associated with the activation of Pi3K–Akt and MAPK/Erk1/2 signaling pathways. Altogether, this causes the inhibition of lipolysis and the activation of glucose uptake in hearts of WT/CKO mice. Activation of β-oxidation and glucose oxidation along with lower activity of complex I lead to the accumulation of NADH, which promotes mitochondrial dysfunction. ( B ) The lower level of canonical Wnt signaling attenuates the cardiomyocytes hypertrophy. Adaptation of WT/CKO mice to the endurance training is accompanied by activation of AMPK and a stronger activation of pre-activated Pi3K–AKT and MAPK/Erk1/2 signaling pathways. Increased AMPK leads to the inhibition of lipolysis and activation of β-oxidation. Activation of AMPK, Pi3K–AKT, and MAPK/Erk1/2 signaling pathways stimulates FA and glucose uptake. Downregulation of canonical Wnt signaling reduces mitochondria biogenesis and OXPHOS activity in the heart during adaptation to the endurance training. Decreased OXPHOS protein level and activity along with enhanced β-oxidation further exacerbate mitochondrial dysfunction. Notes: Red—observed increase; blue—observed decrease; orange—possible increase; green—possible decrease; black—remain unchanged relative to relevant WT/WT mice.

    Article Snippet: Western blot was performed using the following antibodies: β-catenin (1:1000, sc-7963, Santa Cruz Biotechnology, Santa Cruz, CA, USA), Akt1 (1:1000, sc-1618, Santa Cruz Biotechnology), Lef-1 (1:1000, sc-374412, Santa Cruz Biotechnology, Santa Cruz, CA, USA), phosphorylated Akt at Ser473 (1:500, sc-101629, Santa Cruz Biotechnology), phosphorylated Akt at Thr308 (1:500, sc-135650, Santa Cruz Biotechnology, Santa Cruz, CA, USA), Erk1/2 (1:1000, 9102, Cell Signaling Technology, Danvers, MA, USA), phosphorylated Erk1/2 at Thr202 /Thr204 (pErk1/2, 1:1000, 4377, Cell Signaling Technology, Danvers, MA, USA), AMPKα 1/2 (1:500, sc-25792, Santa Cruz Biotechnology), phosphorylated AMPKα at Thr172 (pAMPKα, 1:500, sc-33524-R, Santa Cruz Biotechnology), PKA (1:500, sc-390548, Santa Cruz Biotechnology), phosphorylated PKA (pPKA; 1:500, sc-32968, Santa Cruz Biotechnology), hormone-sensitive lipase (HSL; 1:1000, 4107, Cell Signaling Technology, Danvers, MA, USA), phosphorylated HSL (pHSL) at Ser565 (1:1000, 4137, Cell Signaling Technology, Danvers, MA, USA), pHSL at Ser563 (1:1000, 4139, Cell Signaling Technology, Danvers, MA, USA), acetyl-CoA carboxylase (ACC; 1:1000, 04-322, Millipore, Burlington, MA, USA), phosphorylated ACC (pACC; 1:500, 07-303, Millipore), Axin-1 (1:1000, 3323, Cell Signaling Technology, Danvers, MA, USA), α/β-hydrolase domain (ABHD5, 1:1000, sc-100468, Santa Cruz Biotechnology), adipose triglyceride lipase (ATGL, 1:1000, 2138, Cell Signaling Technology, Danvers, MA, USA), adenomatous polyposis coli (APC, 1:100, sc-896, Santa Cruz Biotechnology), carnitine palmitoyltransferase 1 (CPT1, 1:100, sc-31128, Santa Cruz Biotechnology), CD36 (1:100, sc-9154, Santa Cruz Biotechnology), G0 S2 (1:100, sc-133423, Santa Cruz Biotechnology), GLUT-4 (1:100, sc-7938, Santa Cruz Biotechnology), pyruvate dehydrogenase kinase 1 (PDK1, 1:100, sc-7140, Santa Cruz Biotechnology), mammalian target of rapamycin (mTOR, 1:1000, 2983, Cell Signaling Technology, Danvers, MA, USA), phosphorylated at Ser2448 mTOR (1:1000, 5536, Cell Signaling), OXPHOS (1:1000, ab110413, Abcam, Cambridge, UK) β-actin (1:25,000, A3854, Sigma, St. Louis, MO, USA)and GAPDH (1:25,000, 5174, Cell Signaling) as a loading control.

    Techniques: Knock-Out, Aqueous Normal-phase Chromatography, Activation Assay, Inhibition, Mouse Assay, Activity Assay

    Heterozygous knockout of β-catenin affects hypertrophic signaling in the heart. ( A ) Western blot of pmTOR 2448 , mTOR, pAkt at Thr 308 , pAkt at Ser 473 , Akt, pErk1/2, Erk1/2, phosphorylated PKA (pPKA) and protein kinase A (PKA) in LV lysates from WT/WT and WT/CKO mice in sedentary conditions (Control) and after the endurance training (Training). ( B ) Densitometry of pmTOR at Ser 2448 normalized to mTOR. ( C ) Densitometry of total mTOR normalized to GAPDH. ( D ) Densitometry of pAkt at Ser 473 normalized to Akt. ( E ) Densitometry of pAkt at Thr 308 normalized to Akt. ( F ) Densitometry of total Akt normalized to GAPDH. ( G ) Densitometry of pErk1/2 normalized to total Erk1/2. ( H ) Densitometry of total Erk1/2 normalized to GAPDH. ( I ) Densitometry of pPKA normalized to total PKA. ( J ) Densitometry of total PKA normalized to GAPDH. The data are expressed as the mean ± SD of arbitrary fold of change relative to control levels. n = 5/group. * p

    Journal: Life

    Article Title: β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice

    doi: 10.3390/life10120357

    Figure Lengend Snippet: Heterozygous knockout of β-catenin affects hypertrophic signaling in the heart. ( A ) Western blot of pmTOR 2448 , mTOR, pAkt at Thr 308 , pAkt at Ser 473 , Akt, pErk1/2, Erk1/2, phosphorylated PKA (pPKA) and protein kinase A (PKA) in LV lysates from WT/WT and WT/CKO mice in sedentary conditions (Control) and after the endurance training (Training). ( B ) Densitometry of pmTOR at Ser 2448 normalized to mTOR. ( C ) Densitometry of total mTOR normalized to GAPDH. ( D ) Densitometry of pAkt at Ser 473 normalized to Akt. ( E ) Densitometry of pAkt at Thr 308 normalized to Akt. ( F ) Densitometry of total Akt normalized to GAPDH. ( G ) Densitometry of pErk1/2 normalized to total Erk1/2. ( H ) Densitometry of total Erk1/2 normalized to GAPDH. ( I ) Densitometry of pPKA normalized to total PKA. ( J ) Densitometry of total PKA normalized to GAPDH. The data are expressed as the mean ± SD of arbitrary fold of change relative to control levels. n = 5/group. * p

    Article Snippet: Western blot was performed using the following antibodies: β-catenin (1:1000, sc-7963, Santa Cruz Biotechnology, Santa Cruz, CA, USA), Akt1 (1:1000, sc-1618, Santa Cruz Biotechnology), Lef-1 (1:1000, sc-374412, Santa Cruz Biotechnology, Santa Cruz, CA, USA), phosphorylated Akt at Ser473 (1:500, sc-101629, Santa Cruz Biotechnology), phosphorylated Akt at Thr308 (1:500, sc-135650, Santa Cruz Biotechnology, Santa Cruz, CA, USA), Erk1/2 (1:1000, 9102, Cell Signaling Technology, Danvers, MA, USA), phosphorylated Erk1/2 at Thr202 /Thr204 (pErk1/2, 1:1000, 4377, Cell Signaling Technology, Danvers, MA, USA), AMPKα 1/2 (1:500, sc-25792, Santa Cruz Biotechnology), phosphorylated AMPKα at Thr172 (pAMPKα, 1:500, sc-33524-R, Santa Cruz Biotechnology), PKA (1:500, sc-390548, Santa Cruz Biotechnology), phosphorylated PKA (pPKA; 1:500, sc-32968, Santa Cruz Biotechnology), hormone-sensitive lipase (HSL; 1:1000, 4107, Cell Signaling Technology, Danvers, MA, USA), phosphorylated HSL (pHSL) at Ser565 (1:1000, 4137, Cell Signaling Technology, Danvers, MA, USA), pHSL at Ser563 (1:1000, 4139, Cell Signaling Technology, Danvers, MA, USA), acetyl-CoA carboxylase (ACC; 1:1000, 04-322, Millipore, Burlington, MA, USA), phosphorylated ACC (pACC; 1:500, 07-303, Millipore), Axin-1 (1:1000, 3323, Cell Signaling Technology, Danvers, MA, USA), α/β-hydrolase domain (ABHD5, 1:1000, sc-100468, Santa Cruz Biotechnology), adipose triglyceride lipase (ATGL, 1:1000, 2138, Cell Signaling Technology, Danvers, MA, USA), adenomatous polyposis coli (APC, 1:100, sc-896, Santa Cruz Biotechnology), carnitine palmitoyltransferase 1 (CPT1, 1:100, sc-31128, Santa Cruz Biotechnology), CD36 (1:100, sc-9154, Santa Cruz Biotechnology), G0 S2 (1:100, sc-133423, Santa Cruz Biotechnology), GLUT-4 (1:100, sc-7938, Santa Cruz Biotechnology), pyruvate dehydrogenase kinase 1 (PDK1, 1:100, sc-7140, Santa Cruz Biotechnology), mammalian target of rapamycin (mTOR, 1:1000, 2983, Cell Signaling Technology, Danvers, MA, USA), phosphorylated at Ser2448 mTOR (1:1000, 5536, Cell Signaling), OXPHOS (1:1000, ab110413, Abcam, Cambridge, UK) β-actin (1:25,000, A3854, Sigma, St. Louis, MO, USA)and GAPDH (1:25,000, 5174, Cell Signaling) as a loading control.

    Techniques: Knock-Out, Western Blot, Mouse Assay