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gene exp fabp3 mm02342495 m1  (Thermo Fisher)
99
Thermo Fisher gene exp fabp3 mm02342495 m1
Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) <t>FABP3,</t> (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.
Gene Exp Fabp3 Mm02342495 M1, supplied by Thermo Fisher, 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/product/fabp3/Gene+Exp%2E+Fabp3%2C+Mm02342495_m1/pmc12811436-61-13--1
Average 99 stars, based on 1 article reviews
gene exp fabp3 mm02342495 m1 - by Bioz Stars, 2026-08
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fabp3 antibody  (NSJ Bioreagents)
99
NSJ Bioreagents fabp3 antibody
Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) <t>FABP3,</t> (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.
Fabp3 Antibody, supplied by NSJ Bioreagents, 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/product/fabp3/FABP3+Antibody/custom%40rq4520%4042501785
Average 99 stars, based on 1 article reviews
fabp3 antibody - by Bioz Stars, 2026-08
99/100 stars
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fabp3  (Sanying Ltd)
86
Sanying Ltd fabp3
Validation of DEGs associated with the PPAR signaling pathway by qRT-PCR. ( A-H ) Validation of DEGs related to the PPAR signaling pathway, including CYP4A10 , ACOX2 , SLC27A2 , <t>FABP3</t> , ACAA1B , APOC3 , CYP4A31 , and GK (panels A-H, respectively). The data are presented as mean ± SD, n = 6. Statistical analyses were performed using unpaired Student’s t -test for comparisons between the VCM model group and the VCM + ATO (10 mg/kg) group. In transcriptome sequencing, compared with the VCM model group, ** P < 0.01, *** P < 0.001; in qRT-PCR, compared with the VCM model group, # P < 0.05, ## P < 0.01, ### P < 0.001.
Fabp3, supplied by Sanying Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/fabp3/anti+fabp3/pmc13124441-68-24-28
Average 86 stars, based on 1 article reviews
fabp3 - by Bioz Stars, 2026-08
86/100 stars
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Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) FABP3, (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.

Journal: Journal of Sport and Health Science

Article Title: Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

doi: 10.1016/j.jshs.2025.101095

Figure Lengend Snippet: Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) FABP3, (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.

Article Snippet: The following TaqMan assay gene transcripts were used: fatty acid-binding protein 3 (FABP3, Mm02342495_m1), platelet glycoprotein 4 (CD36, Mm00432403_m1), beta myosin heavy chain (β-MHC, Mm00600555_m1), atrial natriuretic peptide (ANP, Mm01255747_g1), OPA1 (Mm01349707_g1), DRP1 (Mm01342903_m1), robosomal18S (18S, Mm03928990_g1).

Techniques: Staining, Expressing, Binding Assay

Validation of DEGs associated with the PPAR signaling pathway by qRT-PCR. ( A-H ) Validation of DEGs related to the PPAR signaling pathway, including CYP4A10 , ACOX2 , SLC27A2 , FABP3 , ACAA1B , APOC3 , CYP4A31 , and GK (panels A-H, respectively). The data are presented as mean ± SD, n = 6. Statistical analyses were performed using unpaired Student’s t -test for comparisons between the VCM model group and the VCM + ATO (10 mg/kg) group. In transcriptome sequencing, compared with the VCM model group, ** P < 0.01, *** P < 0.001; in qRT-PCR, compared with the VCM model group, # P < 0.05, ## P < 0.01, ### P < 0.001.

Journal: Drug Design, Development and Therapy

Article Title: Atorvastatin Attenuates Vancomycin-Induced Nephrotoxicity via PPARα-Associated Regulation of SLC Transporters

doi: 10.2147/DDDT.S571916

Figure Lengend Snippet: Validation of DEGs associated with the PPAR signaling pathway by qRT-PCR. ( A-H ) Validation of DEGs related to the PPAR signaling pathway, including CYP4A10 , ACOX2 , SLC27A2 , FABP3 , ACAA1B , APOC3 , CYP4A31 , and GK (panels A-H, respectively). The data are presented as mean ± SD, n = 6. Statistical analyses were performed using unpaired Student’s t -test for comparisons between the VCM model group and the VCM + ATO (10 mg/kg) group. In transcriptome sequencing, compared with the VCM model group, ** P < 0.01, *** P < 0.001; in qRT-PCR, compared with the VCM model group, # P < 0.05, ## P < 0.01, ### P < 0.001.

Article Snippet: All antibodies employed in the present study were as follows: Bcl-2 (AF6139, 1:1000 dilution, Affinity Biosciences, USA), Bax (AF0120, 1:1000 dilution, Affinity Biosciences, USA), FABP3 (10,676-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), ACOX2 (17,571-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), FATP2 (14,048-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT1 (26,574-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OCT2 (18,996-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT3 (16,844-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), MATE1 (20,898-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), β-actin (20536-1-AP, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), and horseradish peroxidase (HRP)-conjugated goat anti-rabbit IgG (H + L) secondary antibody (SA00001-2, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China).

Techniques: Biomarker Discovery, Quantitative RT-PCR, Sequencing

Validation of DEGs related to the PPAR signaling pathway and SLC-mediated transmembrane transport by Western blot.Validation of DEGs related to the PPAR signaling pathway by Western blot. ( A ) Western blot analysis of FABP3, ACOX2, and FATP2 protein expression in renal tissues; ( B ) Western blot analysis of OAT1, OCT2, OAT3, and MATE1 protein expression in renal tissues.

Journal: Drug Design, Development and Therapy

Article Title: Atorvastatin Attenuates Vancomycin-Induced Nephrotoxicity via PPARα-Associated Regulation of SLC Transporters

doi: 10.2147/DDDT.S571916

Figure Lengend Snippet: Validation of DEGs related to the PPAR signaling pathway and SLC-mediated transmembrane transport by Western blot.Validation of DEGs related to the PPAR signaling pathway by Western blot. ( A ) Western blot analysis of FABP3, ACOX2, and FATP2 protein expression in renal tissues; ( B ) Western blot analysis of OAT1, OCT2, OAT3, and MATE1 protein expression in renal tissues.

Article Snippet: All antibodies employed in the present study were as follows: Bcl-2 (AF6139, 1:1000 dilution, Affinity Biosciences, USA), Bax (AF0120, 1:1000 dilution, Affinity Biosciences, USA), FABP3 (10,676-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), ACOX2 (17,571-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), FATP2 (14,048-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT1 (26,574-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OCT2 (18,996-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT3 (16,844-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), MATE1 (20,898-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), β-actin (20536-1-AP, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), and horseradish peroxidase (HRP)-conjugated goat anti-rabbit IgG (H + L) secondary antibody (SA00001-2, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China).

Techniques: Biomarker Discovery, Western Blot, Expressing

Mechanistic study of the protective effects of ATO against VIN. ( A ) GW6471 (10 μM) reverses the cytoprotective effect of ATO against VCM-induced injury; ( B ) qRT-PCR analysis of PPARα pathway downstream target genes; ( C ) qRT-PCR analysis of SLC transporter genes. The data are presented as mean ± SD, n = 3. Statistical analyses were performed using Tukey’s post hoc test for all pairwise comparisons. Compared with the CONTROL group, *** P < 0.001; compared with the VCM model group, # P < 0.05, ## P < 0.01, ### P < 0.001; compared with the VCM + ATO (10 μM) group, & P < 0.05, && P < 0.01, &&& P < 0.001. ( A ) CONTROL vs. VCM, P < 0.0001; VCM vs. VCM + ATO (10 μM), P = 0.0002; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0032. (B-FABP3) VCM vs. VCM + ATO (10 μM), P = 0.0028; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0002. (B-AOX2) VCM vs. VCM + ATO (10 μM), P = 0.0055; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0153. (B-SLC27A2) VCM vs. VCM + ATO (10 μM), P = 0.0001; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P < 0.0001. (C-SLC22A6) VCM vs. VCM + ATO (10 μM), P = 0.0115; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0084. (C-SLC22A2) VCM vs. VCM + ATO (10 μM), P < 0.0001; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0001. (C-SLC22A8) VCM vs. VCM + ATO (10 μM), P = 0.0347; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0148. (C-SLC47A1) VCM vs. VCM + ATO (10 μM), P = 0.0034; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0009.

Journal: Drug Design, Development and Therapy

Article Title: Atorvastatin Attenuates Vancomycin-Induced Nephrotoxicity via PPARα-Associated Regulation of SLC Transporters

doi: 10.2147/DDDT.S571916

Figure Lengend Snippet: Mechanistic study of the protective effects of ATO against VIN. ( A ) GW6471 (10 μM) reverses the cytoprotective effect of ATO against VCM-induced injury; ( B ) qRT-PCR analysis of PPARα pathway downstream target genes; ( C ) qRT-PCR analysis of SLC transporter genes. The data are presented as mean ± SD, n = 3. Statistical analyses were performed using Tukey’s post hoc test for all pairwise comparisons. Compared with the CONTROL group, *** P < 0.001; compared with the VCM model group, # P < 0.05, ## P < 0.01, ### P < 0.001; compared with the VCM + ATO (10 μM) group, & P < 0.05, && P < 0.01, &&& P < 0.001. ( A ) CONTROL vs. VCM, P < 0.0001; VCM vs. VCM + ATO (10 μM), P = 0.0002; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0032. (B-FABP3) VCM vs. VCM + ATO (10 μM), P = 0.0028; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0002. (B-AOX2) VCM vs. VCM + ATO (10 μM), P = 0.0055; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0153. (B-SLC27A2) VCM vs. VCM + ATO (10 μM), P = 0.0001; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P < 0.0001. (C-SLC22A6) VCM vs. VCM + ATO (10 μM), P = 0.0115; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0084. (C-SLC22A2) VCM vs. VCM + ATO (10 μM), P < 0.0001; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0001. (C-SLC22A8) VCM vs. VCM + ATO (10 μM), P = 0.0347; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0148. (C-SLC47A1) VCM vs. VCM + ATO (10 μM), P = 0.0034; VCM + ATO (10 μM) vs. VCM + ATO (10 μM) + GW6471, P = 0.0009.

Article Snippet: All antibodies employed in the present study were as follows: Bcl-2 (AF6139, 1:1000 dilution, Affinity Biosciences, USA), Bax (AF0120, 1:1000 dilution, Affinity Biosciences, USA), FABP3 (10,676-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), ACOX2 (17,571-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), FATP2 (14,048-1-AP, 1:2000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT1 (26,574-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OCT2 (18,996-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), OAT3 (16,844-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), MATE1 (20,898-1-AP, 1:1000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), β-actin (20536-1-AP, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China), and horseradish peroxidase (HRP)-conjugated goat anti-rabbit IgG (H + L) secondary antibody (SA00001-2, 1:5000 dilution, SanYing Biotechnology Co., Ltd., Wuhan, China).

Techniques: Quantitative RT-PCR, Control