anti lactate dehydrogenase ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti lactate dehydrogenase ldha
    Anti Lactate Dehydrogenase Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ldha
    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot <t>analyses</t> <t>p-ACC</t> (Ser79), ACC, PDH, and <t>LDHA</t> was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates
    Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "SIRT1 activation promotes energy homeostasis and reprograms liver cancer metabolism"

    Article Title: SIRT1 activation promotes energy homeostasis and reprograms liver cancer metabolism

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-023-04440-9

    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot analyses p-ACC (Ser79), ACC, PDH, and LDHA was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates
    Figure Legend Snippet: SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot analyses p-ACC (Ser79), ACC, PDH, and LDHA was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates

    Techniques Used: Western Blot, Concentration Assay, Expressing, Staining, Standard Deviation

    rabbit anti ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti ldha
    Rabbit Anti Ldha, supplied by Cell Signaling Technology Inc, 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/result/rabbit anti ldha/product/Cell Signaling Technology Inc
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    anti ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ldha
    Anti Ldha, supplied by Cell Signaling Technology Inc, 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/result/anti ldha/product/Cell Signaling Technology Inc
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    ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ldha
    (a) IMR‐90 cells were cultured in normoxic (N) or hypoxic (H) conditions for 5 days, and <t>LDHA</t> <t>and</t> <t>LDHB</t> levels were measured. (b) Upper , Control and IPF fibroblasts ( n = 3 distinct cell lines each) were cultured under the same conditions and LDHA and LDHB protein levels were determined by western blot. GAPDH was used as a loading control. Lower , Quantification of the LDHA/LDHB ratio in Control and IPF fibroblasts was determined by densitometry and expressed by a box‐whisker plot; LDHA and LDHB levels from each control and IPF fibroblast line are shown in the supplemental data section. ** p = 0.0025 compared to normoxic condition.
    Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Persistent hypoxia promotes myofibroblast differentiation via GPR ‐81 and differential regulation of LDH isoenzymes in normal and idiopathic pulmonary fibrosis fibroblasts"

    Article Title: Persistent hypoxia promotes myofibroblast differentiation via GPR ‐81 and differential regulation of LDH isoenzymes in normal and idiopathic pulmonary fibrosis fibroblasts

    Journal: Physiological Reports

    doi: 10.14814/phy2.15759

    (a) IMR‐90 cells were cultured in normoxic (N) or hypoxic (H) conditions for 5 days, and LDHA and LDHB levels were measured. (b) Upper , Control and IPF fibroblasts ( n = 3 distinct cell lines each) were cultured under the same conditions and LDHA and LDHB protein levels were determined by western blot. GAPDH was used as a loading control. Lower , Quantification of the LDHA/LDHB ratio in Control and IPF fibroblasts was determined by densitometry and expressed by a box‐whisker plot; LDHA and LDHB levels from each control and IPF fibroblast line are shown in the supplemental data section. ** p = 0.0025 compared to normoxic condition.
    Figure Legend Snippet: (a) IMR‐90 cells were cultured in normoxic (N) or hypoxic (H) conditions for 5 days, and LDHA and LDHB levels were measured. (b) Upper , Control and IPF fibroblasts ( n = 3 distinct cell lines each) were cultured under the same conditions and LDHA and LDHB protein levels were determined by western blot. GAPDH was used as a loading control. Lower , Quantification of the LDHA/LDHB ratio in Control and IPF fibroblasts was determined by densitometry and expressed by a box‐whisker plot; LDHA and LDHB levels from each control and IPF fibroblast line are shown in the supplemental data section. ** p = 0.0025 compared to normoxic condition.

    Techniques Used: Cell Culture, Western Blot, Whisker Assay

    (a) Representative images of FoxM1 and LDHA levels of IPF or control fibroblasts cultured under hypoxic conditions for 3 days followed by the treatment with 50 nM of either negative control (NC) or FoxM1 (FM1) siRNA for additional 2 days. GAPDH was used as a loading control. (b) Representative images of LDHA levels of control ( n = 3) or IPF fibroblasts ( n = 3) cultured under the hypoxic conditions for 3 days followed by the treatment with 50 nM of negative control (NC) or LDHA (LD) siRNA duplex for additional 2 days. (c) Extracellular lactate concentration (ng/μl) in control ( n = 3) and IPF cells ( n = 4) were measured under the same conditions. The change (%) of lactate in the presence or absence of LDHA siRNA compared to baseline levels under hypoxic conditions (100%) is shown. ** p = 0.0012 compared to lactate levels from NC siRNA transfected IPF fibroblasts.
    Figure Legend Snippet: (a) Representative images of FoxM1 and LDHA levels of IPF or control fibroblasts cultured under hypoxic conditions for 3 days followed by the treatment with 50 nM of either negative control (NC) or FoxM1 (FM1) siRNA for additional 2 days. GAPDH was used as a loading control. (b) Representative images of LDHA levels of control ( n = 3) or IPF fibroblasts ( n = 3) cultured under the hypoxic conditions for 3 days followed by the treatment with 50 nM of negative control (NC) or LDHA (LD) siRNA duplex for additional 2 days. (c) Extracellular lactate concentration (ng/μl) in control ( n = 3) and IPF cells ( n = 4) were measured under the same conditions. The change (%) of lactate in the presence or absence of LDHA siRNA compared to baseline levels under hypoxic conditions (100%) is shown. ** p = 0.0012 compared to lactate levels from NC siRNA transfected IPF fibroblasts.

    Techniques Used: Cell Culture, Negative Control, Concentration Assay, Transfection

    (a) Control ( n = 3) and IPF fibroblasts ( n = 3) were cultured under hypoxic conditions for 4 days and for additional 16 h in the presence or absence of TGF‐β (2 ng/mL). representative α‐SMA, LDHA, and LDHB protein expression in controls (upper) and IPF (lower) are shown. (b) Control and IPF fibroblasts ( n = 3) were cultured in the presence or absence of TGF‐β (2 ng/mL) in the hypoxic chamber. Extracellular lactate concentrations (ng/μL) were measured and expressed as the percentage change compared to baseline in the absence of TGF‐β (100%). *** p = 0.0005.
    Figure Legend Snippet: (a) Control ( n = 3) and IPF fibroblasts ( n = 3) were cultured under hypoxic conditions for 4 days and for additional 16 h in the presence or absence of TGF‐β (2 ng/mL). representative α‐SMA, LDHA, and LDHB protein expression in controls (upper) and IPF (lower) are shown. (b) Control and IPF fibroblasts ( n = 3) were cultured in the presence or absence of TGF‐β (2 ng/mL) in the hypoxic chamber. Extracellular lactate concentrations (ng/μL) were measured and expressed as the percentage change compared to baseline in the absence of TGF‐β (100%). *** p = 0.0005.

    Techniques Used: Cell Culture, Expressing

    anti ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ldha
    a , Schematic of a haploid genetic screen in DGAT DKO cells using the stain BODIPY 493/503. Low and high represent the 5% of cells with the lowest and highest fluorescent signal, respectively. b , Fishtail plot depicting genetic regulators of lipid droplets in a screen of DGAT DKO HAP1 cells. Significant positive and negative regulators are coloured light blue and orange, respectively. The mutational index (MI) represents the ratio of inactivating gene-trap mutations per gene recovered from each (high and low) population (see for a complete description). c , Immunoblot of TMX1 levels in HAP1 cell lines. WB, western <t>blot;</t> <t>PDI,</t> protein disulfide isomerase; <t>LDHA,</t> lactate dehydrogenase A. d , Quantitative increase in lipid droplets (visualized by BODIPY 493/503) in TMX1 -knockout (Δ TMX1 ) HAP1 cells, as measured by flow cytometry. e , Lipid droplets, visualized by BODIPY 665/676 (green in the overlay), in HAP1 cell lines, including a double- DGAT and TMX1 triple knockout (3KO). Blue, Hoechst 33342. Scale bar, 10 μm. f , Lipid droplets (visualized by BODIPY 665/676) in ∆ TMX1 293T cells. Blue, Hoechst 33342. Scale bar, 10 μm. g , TLC of neutral lipids in HAP1 (left) and 293T (right) cell lines. Cells were pulsed with 50 µM oleic acid (OA) for 24 h where indicated. 293T cells were additionally treated with 10 µM (each) DGAT inhibitor (DGATi) where indicated. h , Quantification of the increase in TAG induced by TMX1 deletion in HAP1 and 293T cell lines, normalized to WT cells. Data are mean ± s.e.m. of n = 3 independent experiments (two-way ANOVA, Bonferroni correction; each cell line was analysed separately).
    Anti Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Identification of an alternative triglyceride biosynthesis pathway"

    Article Title: Identification of an alternative triglyceride biosynthesis pathway

    Journal: Nature

    doi: 10.1038/s41586-023-06497-4

    a , Schematic of a haploid genetic screen in DGAT DKO cells using the stain BODIPY 493/503. Low and high represent the 5% of cells with the lowest and highest fluorescent signal, respectively. b , Fishtail plot depicting genetic regulators of lipid droplets in a screen of DGAT DKO HAP1 cells. Significant positive and negative regulators are coloured light blue and orange, respectively. The mutational index (MI) represents the ratio of inactivating gene-trap mutations per gene recovered from each (high and low) population (see for a complete description). c , Immunoblot of TMX1 levels in HAP1 cell lines. WB, western blot; PDI, protein disulfide isomerase; LDHA, lactate dehydrogenase A. d , Quantitative increase in lipid droplets (visualized by BODIPY 493/503) in TMX1 -knockout (Δ TMX1 ) HAP1 cells, as measured by flow cytometry. e , Lipid droplets, visualized by BODIPY 665/676 (green in the overlay), in HAP1 cell lines, including a double- DGAT and TMX1 triple knockout (3KO). Blue, Hoechst 33342. Scale bar, 10 μm. f , Lipid droplets (visualized by BODIPY 665/676) in ∆ TMX1 293T cells. Blue, Hoechst 33342. Scale bar, 10 μm. g , TLC of neutral lipids in HAP1 (left) and 293T (right) cell lines. Cells were pulsed with 50 µM oleic acid (OA) for 24 h where indicated. 293T cells were additionally treated with 10 µM (each) DGAT inhibitor (DGATi) where indicated. h , Quantification of the increase in TAG induced by TMX1 deletion in HAP1 and 293T cell lines, normalized to WT cells. Data are mean ± s.e.m. of n = 3 independent experiments (two-way ANOVA, Bonferroni correction; each cell line was analysed separately).
    Figure Legend Snippet: a , Schematic of a haploid genetic screen in DGAT DKO cells using the stain BODIPY 493/503. Low and high represent the 5% of cells with the lowest and highest fluorescent signal, respectively. b , Fishtail plot depicting genetic regulators of lipid droplets in a screen of DGAT DKO HAP1 cells. Significant positive and negative regulators are coloured light blue and orange, respectively. The mutational index (MI) represents the ratio of inactivating gene-trap mutations per gene recovered from each (high and low) population (see for a complete description). c , Immunoblot of TMX1 levels in HAP1 cell lines. WB, western blot; PDI, protein disulfide isomerase; LDHA, lactate dehydrogenase A. d , Quantitative increase in lipid droplets (visualized by BODIPY 493/503) in TMX1 -knockout (Δ TMX1 ) HAP1 cells, as measured by flow cytometry. e , Lipid droplets, visualized by BODIPY 665/676 (green in the overlay), in HAP1 cell lines, including a double- DGAT and TMX1 triple knockout (3KO). Blue, Hoechst 33342. Scale bar, 10 μm. f , Lipid droplets (visualized by BODIPY 665/676) in ∆ TMX1 293T cells. Blue, Hoechst 33342. Scale bar, 10 μm. g , TLC of neutral lipids in HAP1 (left) and 293T (right) cell lines. Cells were pulsed with 50 µM oleic acid (OA) for 24 h where indicated. 293T cells were additionally treated with 10 µM (each) DGAT inhibitor (DGATi) where indicated. h , Quantification of the increase in TAG induced by TMX1 deletion in HAP1 and 293T cell lines, normalized to WT cells. Data are mean ± s.e.m. of n = 3 independent experiments (two-way ANOVA, Bonferroni correction; each cell line was analysed separately).

    Techniques Used: Staining, Western Blot, Knock-Out, Flow Cytometry, Triple Knockout

    rabbit anti ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti ldha
    Rabbit Anti Ldha, supplied by Cell Signaling Technology Inc, 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/result/rabbit anti ldha/product/Cell Signaling Technology Inc
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    ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ldha
    (A) The mRNA expression levels of <t>LDHA</t> <t>and</t> <t>LDHB</t> in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.
    Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "The novel role of LDHA/LDHB in the prognostic value and tumor-immune infiltration in clear cell renal cell carcinoma"

    Article Title: The novel role of LDHA/LDHB in the prognostic value and tumor-immune infiltration in clear cell renal cell carcinoma

    Journal: PeerJ

    doi: 10.7717/peerj.15749

    (A) The mRNA expression levels of LDHA and LDHB in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.
    Figure Legend Snippet: (A) The mRNA expression levels of LDHA and LDHB in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.

    Techniques Used: Expressing

    (A) Representative immunostaining photomicrographs of LDHA and LDHB expression in ccRCC tissues (IHC). Staining signals displayed cytoplasmic localization of LDHA and LDHB in adjacent normal kidney (left) and ccRCC tissues (middle: low expression, right: high expression). G: ISUP grade, original magnification 200 ×; bars, 50 µm. Kaplan–Meier survival curves demonstrated overall survival of 150 patients with ccRCC, according to LDHA (B) and LDHB (C) staining.
    Figure Legend Snippet: (A) Representative immunostaining photomicrographs of LDHA and LDHB expression in ccRCC tissues (IHC). Staining signals displayed cytoplasmic localization of LDHA and LDHB in adjacent normal kidney (left) and ccRCC tissues (middle: low expression, right: high expression). G: ISUP grade, original magnification 200 ×; bars, 50 µm. Kaplan–Meier survival curves demonstrated overall survival of 150 patients with ccRCC, according to LDHA (B) and LDHB (C) staining.

    Techniques Used: Immunostaining, Expressing, Immunohistochemistry, Staining

    ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ldha
    (A) The mRNA expression levels of <t>LDHA</t> <t>and</t> <t>LDHB</t> in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.
    Ldha, supplied by Cell Signaling Technology Inc, 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/result/ldha/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ldha - by Bioz Stars, 2023-09
    86/100 stars

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    1) Product Images from "The novel role of LDHA/LDHB in the prognostic value and tumor-immune infiltration in clear cell renal cell carcinoma"

    Article Title: The novel role of LDHA/LDHB in the prognostic value and tumor-immune infiltration in clear cell renal cell carcinoma

    Journal: PeerJ

    doi: 10.7717/peerj.15749

    (A) The mRNA expression levels of LDHA and LDHB in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.
    Figure Legend Snippet: (A) The mRNA expression levels of LDHA and LDHB in 523 ccRCC and 100 adjacent normal kidney tissues (GEPIA2, ANOVA test). (B) The protein expression levels of LDHA and LDHB in 100 ccRCC and 84 adjacent normal kidney tissues (UALCAN, ANOVA test). (C) LDHA and LDHB protein expression in seven pairs ccRCC and their adjacent kidney tissues (WB, paired t -test). T, ccRCC; N, normal kidney tissues. * P < 0.05, ** P < 0.01.

    Techniques Used: Expressing

    (A) Representative immunostaining photomicrographs of LDHA and LDHB expression in ccRCC tissues (IHC). Staining signals displayed cytoplasmic localization of LDHA and LDHB in adjacent normal kidney (left) and ccRCC tissues (middle: low expression, right: high expression). G: ISUP grade, original magnification 200 ×; bars, 50 µm. Kaplan–Meier survival curves demonstrated overall survival of 150 patients with ccRCC, according to LDHA (B) and LDHB (C) staining.
    Figure Legend Snippet: (A) Representative immunostaining photomicrographs of LDHA and LDHB expression in ccRCC tissues (IHC). Staining signals displayed cytoplasmic localization of LDHA and LDHB in adjacent normal kidney (left) and ccRCC tissues (middle: low expression, right: high expression). G: ISUP grade, original magnification 200 ×; bars, 50 µm. Kaplan–Meier survival curves demonstrated overall survival of 150 patients with ccRCC, according to LDHA (B) and LDHB (C) staining.

    Techniques Used: Immunostaining, Expressing, Immunohistochemistry, Staining

    rabbit anti ldha  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti ldha
    Rabbit Anti Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti lactate dehydrogenase ldha
    Anti Lactate Dehydrogenase Ldha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot <t>analyses</t> <t>p-ACC</t> (Ser79), ACC, PDH, and <t>LDHA</t> was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates
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    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot <t>analyses</t> <t>p-ACC</t> (Ser79), ACC, PDH, and <t>LDHA</t> was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates
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    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot <t>analyses</t> <t>p-ACC</t> (Ser79), ACC, PDH, and <t>LDHA</t> was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates
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    SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot analyses p-ACC (Ser79), ACC, PDH, and LDHA was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates

    Journal: Journal of Translational Medicine

    Article Title: SIRT1 activation promotes energy homeostasis and reprograms liver cancer metabolism

    doi: 10.1186/s12967-023-04440-9

    Figure Lengend Snippet: SCIC2.1 alters the metabolic program and inhibits lipogenesis upon glucose starvation. Extracellular acidification Rate (ECAR) of HepG2. a Glucose (25 mM) exposure followed by the treatment of SCIC2.1 b Glucose (5 mM) exposure followed by the treatment of SCIC2.1. c Western blot analyses of SCIC2.1 alters the metabolic program upon glucose starvation: Western blot analyses p-ACC (Ser79), ACC, PDH, and LDHA was performed in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated concentration and time points. Heat map showing the band quantification of protein expression. d quantification of Oil Red Oil staining at 540 nm (n = 3) using TECAN in HepG2 cells treated with SCIC2.1 and Ex-527 at indicated time points. e Heat map showing different expression levels of genes involved in glycolysis and lipid metabolism in HepG2 cells treated with SCIC2.1 at 25 µM. Statistical significance was calculated using the student t -test or one-way ANOVA using GraphPad Prism 9.4.0, and statistical significance is expressed as * p -value < 0.05, ** p -value < 0.01, and **** p value < 0.0001 vs control. Error bars represent the standard deviation (SD) of three biological replicates

    Article Snippet: Primary antibodies were: SIRT1 (#8469), Actyl-p53K382 (#2525), FOXO3a (#12,829), UCP2 (#89,326), LDHA (#3582), PUMA (#98,672), p-ACC (ser79, #3661), ACC (#3676), PDH (#2784), GAPDH (#D16H11), and β-Actin (#4967) all purchased from Cell Signaling Technology (Massachusetts, US); p53 (#sc-126) and α-tubulin (#sc-5286) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA); SIRT3 (#ab264041), SIRT6 (#ab88494), Bax (#ab53154), NOX2 (#ab129068), p21 (#ab109520), SOD2 (#ab68155), and anti-Ac-Lys (#ab61257) were purchased from Abcam (Cambridge, UK); phospho-AMPK (Thr183/172, #E-AB21121) was purchased from Elabscience (Texas, US); PGC1α (#PA5-72,948) was purchased from Thermo Fisher Scientific (Massachusetts, US).

    Techniques: Western Blot, Concentration Assay, Expressing, Staining, Standard Deviation