FATP5/SLC27A5 Antibody - BSA Free

Immunohistochemistry-Paraffin: FATP5/SLC27A5 Antibody [NBP1-89267]

Immunohistochemistry-Paraffin: FATP5/SLC27A5 Antibody [NBP1-89267] - Staining of human pancreas shows low expression as expected.

Western Blot: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

SLC27A5 expression is downregulated in the sorafenib-resistant hepatocellular carcinoma cells.A Schematic diagram of the construction of the sorafenib-resistant cells. B The IC50 values of sorafenib-sensitive and sorafenib-resistant SK-Hep1 and HepG2 cells that were incubated with sorafenib in a concentration gradient manner. C, D The mRNA (C) and protein (D) expression of SLC27A5 in sorafenib-sensitive and sorafenib-resistant HCC cells. SR sorafenib resistant. All data are presented as mean +/- SD (n = 3). Statistical significance was calculated using two-tailed unpaired Student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

SLC27A5 depletion activated NRF2/GSR axis in HCC.A, B Representative mRNA levels of NRF2 downstream gene expression in SLC27A5-overexpression (A) and SLC27A5-KO (B) cells under treatment of sorafenib. C Relative mRNA levels of GSR in sorafenib-sensitive (n = 3) and sorafenib-resistant (n = 3) human liver tumors. D Correlation analysis of the mRNA levels of SLC27A5 and GSR in the liver by Spearman. E Histochemical staining for SLC27A5 and GSR in HCC tissues and adjacent non-cancerous tissues. Scale bar: 50 μm. F Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-overexpression SK-Hep1 cultured with sorafenib (10 μM for 24 h) alone or co-treatment with tBHQ (100 μM for 3 h). G Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-KO HepG2 cultured with sorafenib alone or co-treatment with brusatol (40 nM for 24 h). H Kaplan–Meier survival curve analysis based on the expression of SLC27A5 and GSR in the liver tumor. I, J The activity of GSR was determined by the GSR activity kit in SLC27A5-overexpression SK-Hep1 (I) and SLC27A5-KO HepG2 (J). TPM transcripts per million, tBHQ tertiary butylhydroquinone, Bru brusatol. Data shown are mean +/- SD (n = 3). Statistical significance was calculated using two-tailed unpaired Student’s t-test and one-way ANOVA test. *p < 0.05, **p < 0.01 ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

SLC27A5 depletion activated NRF2/GSR axis in HCC.A, B Representative mRNA levels of NRF2 downstream gene expression in SLC27A5-overexpression (A) and SLC27A5-KO (B) cells under treatment of sorafenib. C Relative mRNA levels of GSR in sorafenib-sensitive (n = 3) and sorafenib-resistant (n = 3) human liver tumors. D Correlation analysis of the mRNA levels of SLC27A5 and GSR in the liver by Spearman. E Histochemical staining for SLC27A5 and GSR in HCC tissues and adjacent non-cancerous tissues. Scale bar: 50 μm. F Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-overexpression SK-Hep1 cultured with sorafenib (10 μM for 24 h) alone or co-treatment with tBHQ (100 μM for 3 h). G Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-KO HepG2 cultured with sorafenib alone or co-treatment with brusatol (40 nM for 24 h). H Kaplan–Meier survival curve analysis based on the expression of SLC27A5 and GSR in the liver tumor. I, J The activity of GSR was determined by the GSR activity kit in SLC27A5-overexpression SK-Hep1 (I) and SLC27A5-KO HepG2 (J). TPM transcripts per million, tBHQ tertiary butylhydroquinone, Bru brusatol. Data shown are mean +/- SD (n = 3). Statistical significance was calculated using two-tailed unpaired Student’s t-test and one-way ANOVA test. *p < 0.05, **p < 0.01 ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

BCNU enhances the curative effect of sorafenib in vivo by inducing ferroptosis.A Establishment protocol for the evaluation of tumor growth and resistance of human HepG2-parental and HepG2-SR tumor xenografts in BALB/C nude mice following therapy with sorafenib and BCNU alone or both. B Gross images of the HepG2-derived xenografts in orthotopic implantation model. C, D Analysis of liver/body weight ratio (C) (n = 6) and tumor numbers (D) (n = 6). E, F Relative protein expression of SLC27A5 and GSR in the tumor tissues was assayed by immunohistochemistry (E) and immunoblotting (F). Scale bar: 50 μm. G–I The level of GSR activity (G) (n = 6), GSH/GSSG ratio (H) (n = 6), and ROS (I) (n = 6) were assayed in tumor tissues. Scale bar: 10 μm. Data shown are mean +/- SD. Statistical significance was calculated using one-way ANOVA test. *p < 0.05, **p < 0.01, ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

BCNU enhances the curative effect of sorafenib in vivo by inducing ferroptosis.A Establishment protocol for the evaluation of tumor growth and resistance of human HepG2-parental and HepG2-SR tumor xenografts in BALB/C nude mice following therapy with sorafenib and BCNU alone or both. B Gross images of the HepG2-derived xenografts in orthotopic implantation model. C, D Analysis of liver/body weight ratio (C) (n = 6) and tumor numbers (D) (n = 6). E, F Relative protein expression of SLC27A5 and GSR in the tumor tissues was assayed by immunohistochemistry (E) and immunoblotting (F). Scale bar: 50 μm. G–I The level of GSR activity (G) (n = 6), GSH/GSSG ratio (H) (n = 6), and ROS (I) (n = 6) were assayed in tumor tissues. Scale bar: 10 μm. Data shown are mean +/- SD. Statistical significance was calculated using one-way ANOVA test. *p < 0.05, **p < 0.01, ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: FATP5/SLC27A5 Antibody - BSA Free [NBP1-89267] -

SLC27A5 depletion activated NRF2/GSR axis in HCC.A, B Representative mRNA levels of NRF2 downstream gene expression in SLC27A5-overexpression (A) and SLC27A5-KO (B) cells under treatment of sorafenib. C Relative mRNA levels of GSR in sorafenib-sensitive (n = 3) and sorafenib-resistant (n = 3) human liver tumors. D Correlation analysis of the mRNA levels of SLC27A5 and GSR in the liver by Spearman. E Histochemical staining for SLC27A5 and GSR in HCC tissues and adjacent non-cancerous tissues. Scale bar: 50 μm. F Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-overexpression SK-Hep1 cultured with sorafenib (10 μM for 24 h) alone or co-treatment with tBHQ (100 μM for 3 h). G Relative protein expression of NRF2 and GSR were detected by western blotting in SLC27A5-KO HepG2 cultured with sorafenib alone or co-treatment with brusatol (40 nM for 24 h). H Kaplan–Meier survival curve analysis based on the expression of SLC27A5 and GSR in the liver tumor. I, J The activity of GSR was determined by the GSR activity kit in SLC27A5-overexpression SK-Hep1 (I) and SLC27A5-KO HepG2 (J). TPM transcripts per million, tBHQ tertiary butylhydroquinone, Bru brusatol. Data shown are mean +/- SD (n = 3). Statistical significance was calculated using two-tailed unpaired Student’s t-test and one-way ANOVA test. *p < 0.05, **p < 0.01 ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36635256), licensed under a CC-BY license. Not internally tested by Novus Biologicals.