anti slc27a5  (Boster Bio)

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Ablation of Sympathetic Nerve-β3 Adrenergic Receptor-mediated Adipose Tissue Lipolysis Attenuates Alcohol-induced Liver Injury in Mice

doi: 10.1016/j.jcmgh.2025.101623

Figure Lengend Snippet: Ablation of Adrb3 in adipose tissues attenuates acute alcohol-induced hepatic steatosis. Chow-fed Adrb3 fl/fl and Adrb3 FKO mice were given a single alcohol binge. ( A ) Liver FATP5 protein expression. ( B ) Liver FFA. ( C ) Liver triglyceride. ( D ) Plasma ALT. ( E ) Plasma triglyceride. ( F ) H&E staining of liver tissue sections. Scale bar: 50 μm. ( G ) Oil Red O staining of liver tissue sections. Scale bar: 200 μm. ( H–K ) RT-qPCR was performed using liver samples for the detection of ( H ) SREBP1c, ACC, FASN, and SCD1; ( I ) DGAT1 and DGAT2; ( J ) PPARα, CPT1α, and Acox1; ( K ) ApoB. n = 4–6. Data are expressed as the means ± SEM. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

Article Snippet: Primary antibody FATP5 (#NBP2-37412) was purchased from Novus Biologicals.

Techniques: Expressing, Clinical Proteomics, Staining, Quantitative RT-PCR

Journal: Nature

Article Title: ACLY inhibition promotes tumour immunity and suppresses liver cancer

doi: 10.1038/s41586-025-09297-0

Figure Lengend Snippet: a , Overlay of the extracted ion chromatograms for EVT0185 reaction mixture at 0 and 30 min. b , Mass spectrum of EVT0185-CoA at 30-min. c , Fragment ions of EVT0185-CoA at 30-min sample showing the fragment ion 605 m/z produced following the characteristic neutral loss of 3’-phosphonucleoside diphosphate (507 Da). Western blot showing d , Dkk tag expression in empty vector control (pCMV), SLC27A1 , SLC27A2 , SLC27A4 , and SLC27A5 transfected HEK293 cells e , SLC27A2 (ACSVL1) protein expression in non-transfected cells (lane 1), pCMV controls (lanes 2–4) and SLC27A2 (lanes 5–7) transfected cells; β-actin as a loading control. For gel source data, see Supplementary Fig. . f , Extracted ion chromatogram from the MS1 and MS2 scans of HEK293 cells transfected with SLC27A2 and treated with 30 µM EVT0185. g , Mass spectrum from the MS1 and MS2 scans which shows the parent ion (1112 m/z) and the neutral loss of 3’-phosphonucleoside diphosphate (507 Da), respectively. h , EVT0185-CoA detected only in extracts from HEK293 cells overexpressing SLC27A2 (ACSVL1); mean ± SEM, n = 6 biologically independent samples/group. i , Proportion of human liver cells expressing SLC27A2 mRNA at different stages of disease progression. j , Human SLC27A2 protein expression in different cell types. k , Flow cytometry gating strategy: lymphocyte population identified via FSC vs. SSC, singlets via FSC-A vs. FSC-H, live cells via FSC vs. e780 viability dye, and CD19 + B cells and CD3 + T cells via CD19 vs. CD3 plot. l , PBMCs stimulated with R848 and IL-2 showing CD19 + B cell proliferation compared to negative control. m , Average proliferation index of R848-induced CD19 + B cells with EVT0185 or vehicle, n = 2 biologically independent PBMC donors. n , PBMCs stimulated with Concanavalin A (Con A) and IL-2 showing CD3 + T cell proliferation compared to negative control. o , Average proliferation index of Con A-induced CD3 + T cells with EVT0185 or vehicle, n = 2 biologically independent PBMC donors.

Article Snippet: HEK293 cells were transfected with expression plasmid for SLC27A1 ( NM_198580 , human tagged ORF clone; RC209285, OriGene), SLC27A2 ( NM_003645 , human tagged ORF clone; RC221033, OriGene), SLC27A4 ( NM_005094 , human tagged ORF clone; RC209557, OriGene), SLC27A5 ( NM_012254 , human tagged ORF clone; RC215758, Origene) or control vector (pCMV6-entry mammalian expression vector; PS100001, OriGene).

Techniques: Produced, Western Blot, Expressing, Plasmid Preparation, Control, Transfection, Biomarker Discovery, Flow Cytometry, Negative Control

Journal: Scientific Reports

Article Title: Intriguing hepatoprotective effects of sucrose on hepatocellular carcinoma pathogenesis

doi: 10.1038/s41598-024-74991-4

Figure Lengend Snippet: Genes related to oxidative stress response and lipid regulation. ( a ) Protein-protein interaction network illustrating key regulators of oxidative stress and lipid metabolism. ( b ) mRNA expression levels: Pgc1a decreased in all groups vs. 18-C, while Pgc1b showed no significant changes. PPRC1 significantly increased during the neoplastic period (18-18-D/S). Sucrose co-administration (18-6-D/S and 18-18-D/S) led to marked differences in Fabp1 and Cav1 expression vs. 18-DEN. ( c ) Disease-free progression in HCC patients: Alterations in genes such as PPARGC1A, PPARGC1B, PPRC1, PPARA, PPARD, PPARG, SLC27A5, FABP1, CAV1, and CD36 correlated with increased disease progression compared to patients without these gene alterations . FC Fold change.

Article Snippet: TaqMan ® gene expression assays were used in the QuantStudio 7 Flex Real-time PCR system (Applied Biosystem, MA, USA) to evaluate the expression of the following rat genes, Ggt1 (Rn00587709_m1), Gstp1 (Rn00561378_gH), Keap1 (Rn00589292_m1), and Nfe2l2 (Rn00477784_m1), Ppargc1a (Rn00580241_m1), Ppargc1b (Rn00598552_m1), Pprc1 (Rn01411002_m1), Ppara (Rn00566193_m1), Ppard (Rn00565707_m1), Pparg (Rn00440945 _m1), Slc27a5 (Rn00577177_m1), Fabp1 (Rn00664587_m1), Cd36 (Rn00580728_m1) and Cav1 (Rn00755834_m1).

Techniques: Expressing, Biomarker Discovery

Journal: Aging

Article Title: Copper metabolism-related risk score identifies hepatocellular carcinoma subtypes and SLC27A5 as a potential regulator of cuproptosis.

doi: 10.18632/aging.205334

Figure Lengend Snippet: Figure 8. The expression and function of SLC27A5 in HCC. (A–C) The transcriptional expression of SLC27A5 in HCC and normal tissues of TCGA-LIHC (A), GSE14520 (B) and GSE64041 (C) datasets. (D) The protein level of SLC27A5 in HCC and normal tissues. (E, F) CCK-8 assay for HepG2 (E) and LM-3 (F) cells overexpressing SL27A5. (G, H) HepG2 (G) and LM-3 (H) cells were subject to flow cytometry analysis for cell cycle. (I) HCC cells overexpressing SLC27A5 were subject to EdU staining. (J) HCC cells overexpressing SLC27A5 were subject to wound healing assay.

Article Snippet: Western blotting was performed using antibodies against FDX1 (M05441, Boster), SLC27A5 (A09287-2, Boster), GAPDH (BM3876, Boster).

Techniques: Expressing, CCK-8 Assay, Flow Cytometry, Staining, Wound Healing Assay

Journal: Aging

Article Title: Copper metabolism-related risk score identifies hepatocellular carcinoma subtypes and SLC27A5 as a potential regulator of cuproptosis.

doi: 10.18632/aging.205334

Figure Lengend Snippet: Figure 9. SLC27A5 upregulates FDX1 in HCC. (A, B) The correlation between the expression of SLC27A5 and that of FDX1 in TCGA-LIHC (A) and GSE14520 (B) datasets. (C) Dot plot showing the dependency scores for SLC27A5 and FDX1 across all tumor cell lines in the Project Achilles/Cancer Dependency Map Portal (DepMap). (D, E) The expression of and correlation between SLC27A5 and FDX1 in collected HCC tissue chip. (F, G) HepG2 (F) and LM-3 (G) cells overexpressing SLC27A5 were subject to qRT-PCR analysis. (H, I) Western blotting using lysates of HepG2 (H) and LM-3 (I) cells after overexpressing SLC27A5.

Article Snippet: Western blotting was performed using antibodies against FDX1 (M05441, Boster), SLC27A5 (A09287-2, Boster), GAPDH (BM3876, Boster).

Techniques: Expressing, Quantitative RT-PCR, Western Blot

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 2. SLC27A5 deficiency in mice develops liver fibrosis after 24 months of age A) Representative pictures of livers from 24-month-old WT and Slc27a5−/−mice. Scale bar, 2 mm. B) Serum ALT, AST, and ALP levels from 24-month-old WT and Slc27a5−/−mice (n = 5 per group). C) Representative images of H&E and Sirius Red staining from liver tissues of WT and Slc27a5−/−mice at 12, 18, and 24 months (n = 5 per group). Scale bar, 50 μm. D) Quantification of Sirius red staining is described in (C). E,F) Relative mRNA levels of profibrotic genes (E) and inflammatory genes (F) of liver tissues from 24-month-old WT and Slc27a5−/−mice (n = 5 per group). G) The hepatic mRNA levels of gene expression of bile acids synthesis in 24-month-old WT and Slc27a5−/−mice (n = 5 per group). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ns., not significant, two-tailed Student’s t test.

Article Snippet: After blocking in 5% milk for 1 h, the membranes were probed with primary antibodies against SLC27A5 (1:1000, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:1000, ER1003, Huabio, Hangzhou, China), COL1A1 (1:1000, WL0088, Wanleibio, Shenyang, China), COL3A1 (1:1000, 22734-1-AP, Proteintech, IL, USA), RUNX2 (1:1000, 20700-1-AP, Proteintech, IL, USA), EGR3 (1:500, sc-390967, Santa Cruz Biotechnology, USA), β-actin (1:3000, BL005B, Biosharp), or GAPDH (1:3000, AG019-1, Beyotime, Shanghai, China) at 4 °C overnight.

Techniques: Staining, Gene Expression, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 3. SLC27A5 deficiency promotes CCl4- and TAA-induced liver fibrosis in mice A–D) Eight-week-old male WT and Slc27a5−/−mice were injected with CCl4 for six weeks (n = 5 per group). E–H) Eight-week-old male WT and Slc27a5−/−mice were injected with TAA for eight weeks (n = 5 per group). (A,E) The experimental approach of the animal model establishment. (B,F) Representative histology of H&E, Sirius Red, and IHC staining (𝛼-SMA, F4/80) from each group. Scale bar, 50 μm. (C) Quantification of Sirius red, F4/80, and 𝛼-SMA IHC staining are described in (B). G) Quantification of Sirius red, F4/80, and 𝛼-SMA IHC staining are described in (F). (D,H) Serum levels of ALT, AST, and ALP were measured. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed Student’s t test.

Article Snippet: After blocking in 5% milk for 1 h, the membranes were probed with primary antibodies against SLC27A5 (1:1000, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:1000, ER1003, Huabio, Hangzhou, China), COL1A1 (1:1000, WL0088, Wanleibio, Shenyang, China), COL3A1 (1:1000, 22734-1-AP, Proteintech, IL, USA), RUNX2 (1:1000, 20700-1-AP, Proteintech, IL, USA), EGR3 (1:500, sc-390967, Santa Cruz Biotechnology, USA), β-actin (1:3000, BL005B, Biosharp), or GAPDH (1:3000, AG019-1, Beyotime, Shanghai, China) at 4 °C overnight.

Techniques: Injection, Animal Model, Immunohistochemistry, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 5. Elevation of unconjugated CA promotes HSCs activation. A) Serum CA and DCA levels in Slc27a5−/−and WT mice at 24 months of age (n = 5 per group). B) Liver CA and DCA levels in Slc27a5−/−and WT mice at 24 months of age (n = 5 per group). C) LX-2 cells were treated with CA at 25, 50, and 100 μм for 48 h. The expression of 𝛼-SMA was measured using immunostaining. D–F) WT mice HSCs were treated with CA at 50 μм for 48 h. mRNA expression of fibrogenic genes (D), protein expression of 𝛼-SMA, COL1A1, and COL3A1 (E), and 𝛼-SMA immunostaining (F) are displayed. G) The serum levels of CA and DCA in healthy individuals and patients with cirrhosis (n = 18 per group). H) CA levels were measured in media from parental and SLC27A5-KO MIHA cells (n = 3 per group). I) CA levels were measured in PMHs supernatant from WT and Slc27a5−/−mice (n = 3 per group). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed Student’s t test.

Article Snippet: After blocking in 5% milk for 1 h, the membranes were probed with primary antibodies against SLC27A5 (1:1000, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:1000, ER1003, Huabio, Hangzhou, China), COL1A1 (1:1000, WL0088, Wanleibio, Shenyang, China), COL3A1 (1:1000, 22734-1-AP, Proteintech, IL, USA), RUNX2 (1:1000, 20700-1-AP, Proteintech, IL, USA), EGR3 (1:500, sc-390967, Santa Cruz Biotechnology, USA), β-actin (1:3000, BL005B, Biosharp), or GAPDH (1:3000, AG019-1, Beyotime, Shanghai, China) at 4 °C overnight.

Techniques: Activation Assay, Expressing, Immunostaining, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 8. Underlying mechanisms of SLC27A5 deficiency promotes HSCs activation and fibrosis via CA. SLC27A5 was downregulated in liver fibro- sis tissues via RUNX2. The loss of SLC27A5 in mice resulted in accumu- lating unconjugated CA in hepatocytes and subsequently activated HSCs via EGR3. Re-expression of SLC27A5 or inhibition of CA accumulation may represent a potential strategy for liver fibrosis treatment. SLC27A5, solute carrier family 27 member 5; RUNX2, RUNX family transcription factor 2; CA, cholic acid; TCA, taurocholic acid; BSH, bile salt hydrolases; ASBT, api- cal sodium-dependent bile acid transporter; EGR3, early growth response protein 3; HSC, hepatic stellate cell.

Article Snippet: After blocking in 5% milk for 1 h, the membranes were probed with primary antibodies against SLC27A5 (1:1000, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:1000, ER1003, Huabio, Hangzhou, China), COL1A1 (1:1000, WL0088, Wanleibio, Shenyang, China), COL3A1 (1:1000, 22734-1-AP, Proteintech, IL, USA), RUNX2 (1:1000, 20700-1-AP, Proteintech, IL, USA), EGR3 (1:500, sc-390967, Santa Cruz Biotechnology, USA), β-actin (1:3000, BL005B, Biosharp), or GAPDH (1:3000, AG019-1, Beyotime, Shanghai, China) at 4 °C overnight.

Techniques: Activation Assay, Expressing, Inhibition

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 2. SLC27A5 deficiency in mice develops liver fibrosis after 24 months of age A) Representative pictures of livers from 24-month-old WT and Slc27a5−/−mice. Scale bar, 2 mm. B) Serum ALT, AST, and ALP levels from 24-month-old WT and Slc27a5−/−mice (n = 5 per group). C) Representative images of H&E and Sirius Red staining from liver tissues of WT and Slc27a5−/−mice at 12, 18, and 24 months (n = 5 per group). Scale bar, 50 μm. D) Quantification of Sirius red staining is described in (C). E,F) Relative mRNA levels of profibrotic genes (E) and inflammatory genes (F) of liver tissues from 24-month-old WT and Slc27a5−/−mice (n = 5 per group). G) The hepatic mRNA levels of gene expression of bile acids synthesis in 24-month-old WT and Slc27a5−/−mice (n = 5 per group). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ns., not significant, two-tailed Student’s t test.

Article Snippet: Sections were immune-stained for SLC27A5 (1:500, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:300, 19245T, CST, MA, USA), F4/80 (1:300, 70076T, CST), or RUNX2 (1:300, 20700-1-AP, Proteintech, IL, USA) overnight at 4 °C.

Techniques: Staining, Gene Expression, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 3. SLC27A5 deficiency promotes CCl4- and TAA-induced liver fibrosis in mice A–D) Eight-week-old male WT and Slc27a5−/−mice were injected with CCl4 for six weeks (n = 5 per group). E–H) Eight-week-old male WT and Slc27a5−/−mice were injected with TAA for eight weeks (n = 5 per group). (A,E) The experimental approach of the animal model establishment. (B,F) Representative histology of H&E, Sirius Red, and IHC staining (𝛼-SMA, F4/80) from each group. Scale bar, 50 μm. (C) Quantification of Sirius red, F4/80, and 𝛼-SMA IHC staining are described in (B). G) Quantification of Sirius red, F4/80, and 𝛼-SMA IHC staining are described in (F). (D,H) Serum levels of ALT, AST, and ALP were measured. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed Student’s t test.

Article Snippet: Sections were immune-stained for SLC27A5 (1:500, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:300, 19245T, CST, MA, USA), F4/80 (1:300, 70076T, CST), or RUNX2 (1:300, 20700-1-AP, Proteintech, IL, USA) overnight at 4 °C.

Techniques: Injection, Animal Model, Immunohistochemistry, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 5. Elevation of unconjugated CA promotes HSCs activation. A) Serum CA and DCA levels in Slc27a5−/−and WT mice at 24 months of age (n = 5 per group). B) Liver CA and DCA levels in Slc27a5−/−and WT mice at 24 months of age (n = 5 per group). C) LX-2 cells were treated with CA at 25, 50, and 100 μм for 48 h. The expression of 𝛼-SMA was measured using immunostaining. D–F) WT mice HSCs were treated with CA at 50 μм for 48 h. mRNA expression of fibrogenic genes (D), protein expression of 𝛼-SMA, COL1A1, and COL3A1 (E), and 𝛼-SMA immunostaining (F) are displayed. G) The serum levels of CA and DCA in healthy individuals and patients with cirrhosis (n = 18 per group). H) CA levels were measured in media from parental and SLC27A5-KO MIHA cells (n = 3 per group). I) CA levels were measured in PMHs supernatant from WT and Slc27a5−/−mice (n = 3 per group). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed Student’s t test.

Article Snippet: Sections were immune-stained for SLC27A5 (1:500, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:300, 19245T, CST, MA, USA), F4/80 (1:300, 70076T, CST), or RUNX2 (1:300, 20700-1-AP, Proteintech, IL, USA) overnight at 4 °C.

Techniques: Activation Assay, Expressing, Immunostaining, Two Tailed Test

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

doi: 10.1002/advs.202304408

Figure Lengend Snippet: Figure 8. Underlying mechanisms of SLC27A5 deficiency promotes HSCs activation and fibrosis via CA. SLC27A5 was downregulated in liver fibro- sis tissues via RUNX2. The loss of SLC27A5 in mice resulted in accumu- lating unconjugated CA in hepatocytes and subsequently activated HSCs via EGR3. Re-expression of SLC27A5 or inhibition of CA accumulation may represent a potential strategy for liver fibrosis treatment. SLC27A5, solute carrier family 27 member 5; RUNX2, RUNX family transcription factor 2; CA, cholic acid; TCA, taurocholic acid; BSH, bile salt hydrolases; ASBT, api- cal sodium-dependent bile acid transporter; EGR3, early growth response protein 3; HSC, hepatic stellate cell.

Article Snippet: Sections were immune-stained for SLC27A5 (1:500, NBP2-37412, Novus Biologicals, CO, USA), α-SMA (1:300, 19245T, CST, MA, USA), F4/80 (1:300, 70076T, CST), or RUNX2 (1:300, 20700-1-AP, Proteintech, IL, USA) overnight at 4 °C.

Techniques: Activation Assay, Expressing, Inhibition