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Santa Cruz Biotechnology mct1
Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) <t>MCT1,</t> MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.
Mct1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 269 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer"

Article Title: Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer

Journal: iScience

doi: 10.1016/j.isci.2026.115112

Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) MCT1, MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.
Figure Legend Snippet: Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) MCT1, MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.

Techniques Used: Expressing, Western Blot, Control



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Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) <t>MCT1,</t> MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.
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Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) <t>MCT1,</t> MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.
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G-protein-coupled receptor 81 (GPR81) may regulate <t>monocarboxylate</t> <t>transporter</t> <t>1</t> <t>(MCT1)</t> expression in hepatocytes in vitro . (A) Alpha mouse liver 12 (AML12) cells were treated with sodium L-lactate 20 and 40 mM for different time course. Western blot analysis was performed to assess the expression levels of GPR81, MCT1, and MCT4 in AML12 cells. (B) AML12 cells were treated with small interfering RNA (siRNA) 50 nM with or without lactate 20 mM for 3 days. Western blot analysis was conducted to evaluate the expression levels of GPR81 and MCT1 in AML12 cells. The intensities of the bands in the Western blot images were quantified using Image Lab software and are displayed in the corresponding plot alongside the representative blot images. The protein levels were normalized to β-actin expression. Statistical significance compared with control is indicated by a P <0.05, b P <0.01, c P <0.001, lactate 20 mM treated group vs. control; d P <0.05, e P <0.01, f P <0.001, lactate 40 mM treated group vs. control; statistical significance compared with si-scramble is indicated by g P <0.05, h P <0.01, i P <0.001, with siGPR81 indicated j P <0.01.
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Image Search Results


Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) MCT1, MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.

Journal: iScience

Article Title: Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer

doi: 10.1016/j.isci.2026.115112

Figure Lengend Snippet: Acid adaptation and p53 KO alter protein expression of acid-base transporters At week 11, WT and p53KO organoids grown under Ctrl, AA, or AA->7.4 conditions as in were lysed and subjected to western blot analysis for proteins relevant to acid-base homeostasis. Representative western blots are shown on the left, panels on the right show the corresponding densitometric quantifications, as means with S.E.M. error bars and biological replicates shown as open circles. β-actin is used as loading control. A(i) NHE1, NBCn1 western blots, (ii) and (iii), Quantifications of relative NHE1 and NBCn1 levels, respectively. B(i) MCT1, MCT4 western blots, (ii) and (iii), Quantifications of relative MCT1 and MCT4 levels, respectively. C(i) Slc26a6, CFTR western blots, (ii) and (iii), Quantifications of relative Slc26a6 and CFTR levels, respectively. Data represent 3–8 independent biological repeats per condition/protein. Statistical analysis: two-way ANOVA, with Tukey’s post test.

Article Snippet: MCT1 , Santa Cruz Biotechnology , Sc-365501, RRID: AB_2943297.

Techniques: Expressing, Western Blot, Control

G-protein-coupled receptor 81 (GPR81) may regulate monocarboxylate transporter 1 (MCT1) expression in hepatocytes in vitro . (A) Alpha mouse liver 12 (AML12) cells were treated with sodium L-lactate 20 and 40 mM for different time course. Western blot analysis was performed to assess the expression levels of GPR81, MCT1, and MCT4 in AML12 cells. (B) AML12 cells were treated with small interfering RNA (siRNA) 50 nM with or without lactate 20 mM for 3 days. Western blot analysis was conducted to evaluate the expression levels of GPR81 and MCT1 in AML12 cells. The intensities of the bands in the Western blot images were quantified using Image Lab software and are displayed in the corresponding plot alongside the representative blot images. The protein levels were normalized to β-actin expression. Statistical significance compared with control is indicated by a P <0.05, b P <0.01, c P <0.001, lactate 20 mM treated group vs. control; d P <0.05, e P <0.01, f P <0.001, lactate 40 mM treated group vs. control; statistical significance compared with si-scramble is indicated by g P <0.05, h P <0.01, i P <0.001, with siGPR81 indicated j P <0.01.

Journal: Diabetes & Metabolism Journal

Article Title: Lactate-Induced Lipid Accumulation in Hepatocytes through GPR81 Activation

doi: 10.4093/dmj.2024.0531

Figure Lengend Snippet: G-protein-coupled receptor 81 (GPR81) may regulate monocarboxylate transporter 1 (MCT1) expression in hepatocytes in vitro . (A) Alpha mouse liver 12 (AML12) cells were treated with sodium L-lactate 20 and 40 mM for different time course. Western blot analysis was performed to assess the expression levels of GPR81, MCT1, and MCT4 in AML12 cells. (B) AML12 cells were treated with small interfering RNA (siRNA) 50 nM with or without lactate 20 mM for 3 days. Western blot analysis was conducted to evaluate the expression levels of GPR81 and MCT1 in AML12 cells. The intensities of the bands in the Western blot images were quantified using Image Lab software and are displayed in the corresponding plot alongside the representative blot images. The protein levels were normalized to β-actin expression. Statistical significance compared with control is indicated by a P <0.05, b P <0.01, c P <0.001, lactate 20 mM treated group vs. control; d P <0.05, e P <0.01, f P <0.001, lactate 40 mM treated group vs. control; statistical significance compared with si-scramble is indicated by g P <0.05, h P <0.01, i P <0.001, with siGPR81 indicated j P <0.01.

Article Snippet: Subsequently, the AML12 cells were incubated overnight at 4°C with the primary antibody for MCT1 (1:50; sc-365501, Santa Cruz Biotechnology).

Techniques: Expressing, In Vitro, Western Blot, Small Interfering RNA, Software, Control

G-protein-coupled receptor 81 (GPR81) played a major role in regulating lipid accumulation in lactate-treated alpha mouse liver 12 (AML12) cells. (A) AML12 cells were treated with L-lactate at 20 mM with or without AZD3965 at 100 nM for 4 days. Lipid accumulation was evaluated using Oil Red O staining. (B) AML12 cells were treated with sodium L-lactate 20 and 40 mM for 3 days. The isolation of plasma membrane (PM) and cytosol fractions was performed, and the expression of GPR81 and monocarboxylate transporter 1 (MCT1) in AML12 cells was assessed. Na/K ATPase served as a housekeeping marker for the PM, while tubulin served as a housekeeping marker for the cytosol. (C) Immunofluorescence of MCT1 (red) and nuclei (4ʹ,6-diamidino2-phenylindole [DAPI] blue). Scale bar: 20 μm. (D) AML12 cells were treated with small interfering RNA (siRNA) 50 nM with or without lactate 20 mM for 4 days. The accumulation of lipids in AML12 cells was visualized using Oil Red O staining. Statistical significance compared with control is indicated by a P <0.05, b P <0.01. Statistical significance compared with si-scramble is indicated by c P <0.05, d P <0.001, with siGPR81 indicated e P <0.001.

Journal: Diabetes & Metabolism Journal

Article Title: Lactate-Induced Lipid Accumulation in Hepatocytes through GPR81 Activation

doi: 10.4093/dmj.2024.0531

Figure Lengend Snippet: G-protein-coupled receptor 81 (GPR81) played a major role in regulating lipid accumulation in lactate-treated alpha mouse liver 12 (AML12) cells. (A) AML12 cells were treated with L-lactate at 20 mM with or without AZD3965 at 100 nM for 4 days. Lipid accumulation was evaluated using Oil Red O staining. (B) AML12 cells were treated with sodium L-lactate 20 and 40 mM for 3 days. The isolation of plasma membrane (PM) and cytosol fractions was performed, and the expression of GPR81 and monocarboxylate transporter 1 (MCT1) in AML12 cells was assessed. Na/K ATPase served as a housekeeping marker for the PM, while tubulin served as a housekeeping marker for the cytosol. (C) Immunofluorescence of MCT1 (red) and nuclei (4ʹ,6-diamidino2-phenylindole [DAPI] blue). Scale bar: 20 μm. (D) AML12 cells were treated with small interfering RNA (siRNA) 50 nM with or without lactate 20 mM for 4 days. The accumulation of lipids in AML12 cells was visualized using Oil Red O staining. Statistical significance compared with control is indicated by a P <0.05, b P <0.01. Statistical significance compared with si-scramble is indicated by c P <0.05, d P <0.001, with siGPR81 indicated e P <0.001.

Article Snippet: Subsequently, the AML12 cells were incubated overnight at 4°C with the primary antibody for MCT1 (1:50; sc-365501, Santa Cruz Biotechnology).

Techniques: Staining, Isolation, Clinical Proteomics, Membrane, Expressing, Marker, Immunofluorescence, Small Interfering RNA, Control