ldha Search Results


96
Thermo Fisher gene exp ldha mm01612132 g1
a Scheme for the generation of an inducible β-cell-specific TBL1X and TBL1XR1 knockout. b Random fed blood glucose levels over time in iTBL/RβKO ( n = 9) and control ( n = 9) mice on HFD. c Total pancreas insulin content normalized to protein levels in iTBL/RβKO and control mice 4 and 11 weeks after tamoxifen administration. n = 3 for 4w control and iTBL/RβKO mice, n = 6 for 11w control mice, n = 4 for 11w iTBL/RβKO mice. d , e Blood glucose ( d ) and plasma insulin ( e ) levels during an oral glucose tolerance test after 22 weeks of HFD. Corresponding area under the curve in iTBL/RβKO ( n = 8) and control ( n = 9) mice ( d , right). f , g Relative mRNA expression determined by qPCR in pancreatic islets of iTBL/RβKO and control mice of Tbl1x and Tbl1xr1 ( f ) and islet genes ( g ). Control mice Tbl1x , Tbl1xr1 , Ins1 , Ins2 , Nkx6.1 , Slc2a2 , Mafa , Pdx1 , Pax6 , Ucn3 : n = 9, control mice ChgA , Ngn3 , <t>Ldha</t> , Hk1 : n = 8, iTBL/RβKO mice Tbl1x , Ngn3 , Ldha , Hk1 : n = 7, iTBL/RβKO mice Tbl1xr1 , Ins1 , Ins2 , Slc2a2 , Mafa n = 6, iTBL/RβKO mice Nkx6.1 , Pdx1 , Pax6 , Ucn3 , ChgA : n = 5. h α/β-cell mass ratio of pancreatic islets from iTBL/RβKO ( n = 4) and control mice ( n = 4) on HFD, 24 weeks after knockout induction. i Representative immunofluorescent staining of insulin + (blue, β-cells) and glucagon + (red, α-cells) cells of paraffin-embedded pancreas from iTBL/RβKO and control mice on HFD, 24 weeks after knockout induction. Each point represents one mouse. Data are represented as mean ± SEM. The following statistical tests were applied: two-sided student’s t test ( d – Area under the curve, f – h ) and 2-way ANOVA with Šidák’s multiple comparison post hoc test ( b – d – time course, e ). Source data are provided as a Source Data file.
Gene Exp Ldha Mm01612132 G1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Novus Biologicals ldha
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Ldha, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Elabscience Biotechnology human ldha
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Human Ldha, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
OriGene mouse monoclonal ldha antibody
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Mouse Monoclonal Ldha Antibody, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
R&D Systems anti mouse recombinant ldha purified sheep igg
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Anti Mouse Recombinant Ldha Purified Sheep Igg, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
Proteintech lactate dehydrogenase ldh
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Lactate Dehydrogenase Ldh, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals rabbit anti ldh a
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Rabbit Anti Ldh A, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
Proteintech anti ldha
HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, <t>LDHA</t> , and SLC2A1 <t>(</t> <t>GLUT1</t> ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.
Anti Ldha, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
OriGene type ldha
Figure 1. Cisplatin (CDDP) treatments decrease lactate dehydrogenase‑A <t>(LDHA)</t> expression. (A) CDDP treatments at 5, 10 and 50 µM in OECM‑1 and H‑1 cells decreased the level of LDHA expression. β‑actin served as a loading control. (B) Generation of the CDDP‑resistant cell line. OECM‑1 CDDP‑sensitive (Cis S) and CDDP‑resistant (Cis R) cells were treated at 10, 50 and 100 µM CDDP, followed by the measurement of cell viability. (C) Cis R clone number 1 (C1), and Cis R clone number 2 (C2) and the Cis R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represents the mean of three independent experiments and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.
Type Ldha, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals nbp1 47822
Figure 1. Cisplatin (CDDP) treatments decrease lactate dehydrogenase‑A <t>(LDHA)</t> expression. (A) CDDP treatments at 5, 10 and 50 µM in OECM‑1 and H‑1 cells decreased the level of LDHA expression. β‑actin served as a loading control. (B) Generation of the CDDP‑resistant cell line. OECM‑1 CDDP‑sensitive (Cis S) and CDDP‑resistant (Cis R) cells were treated at 10, 50 and 100 µM CDDP, followed by the measurement of cell viability. (C) Cis R clone number 1 (C1), and Cis R clone number 2 (C2) and the Cis R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represents the mean of three independent experiments and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.
Nbp1 47822, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ldha/pm22659615-36-6-3?v=Novus+Biologicals
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93
OriGene ldha plasmid
(A) Immunoblot showing overexpression of <t>LDHA</t> at 5 and 10 mg concentration of the LDHA plasmid in U87 cells, represented with LDHA and Myc tag LDHA. Quantification of the percentage of overexpression observed. (B) Cell viability of control, empty vector, and LDHA plasmid overexpression. Cell viability graphs of STP, TMZ, and GSK without overexpression of LDHA and with overexpression of LDHA. (C) Immunoblot representing LDHA knockdown <t>by</t> <t>siLDHA.</t> Quantification of the percentage decrease in LDHA expression. (D) Cell viability analysis of STP, TMZ, and GSK upon knockdown of LDHA. (E) Kinetic evaluation of LDHA enzyme activity assay with STP, and sodium oxamate. (F) Cell viability of SKNSH cells upon treatment with STP and Diazepam. n=3, *p<0.033, **p<0.002, ***p<0.001, one-way ANOVA Tukey test.
Ldha Plasmid, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Cyagen Biosciences ldha flox
(A) Immunoblot showing overexpression of <t>LDHA</t> at 5 and 10 mg concentration of the LDHA plasmid in U87 cells, represented with LDHA and Myc tag LDHA. Quantification of the percentage of overexpression observed. (B) Cell viability of control, empty vector, and LDHA plasmid overexpression. Cell viability graphs of STP, TMZ, and GSK without overexpression of LDHA and with overexpression of LDHA. (C) Immunoblot representing LDHA knockdown <t>by</t> <t>siLDHA.</t> Quantification of the percentage decrease in LDHA expression. (D) Cell viability analysis of STP, TMZ, and GSK upon knockdown of LDHA. (E) Kinetic evaluation of LDHA enzyme activity assay with STP, and sodium oxamate. (F) Cell viability of SKNSH cells upon treatment with STP and Diazepam. n=3, *p<0.033, **p<0.002, ***p<0.001, one-way ANOVA Tukey test.
Ldha Flox, supplied by Cyagen Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


a Scheme for the generation of an inducible β-cell-specific TBL1X and TBL1XR1 knockout. b Random fed blood glucose levels over time in iTBL/RβKO ( n = 9) and control ( n = 9) mice on HFD. c Total pancreas insulin content normalized to protein levels in iTBL/RβKO and control mice 4 and 11 weeks after tamoxifen administration. n = 3 for 4w control and iTBL/RβKO mice, n = 6 for 11w control mice, n = 4 for 11w iTBL/RβKO mice. d , e Blood glucose ( d ) and plasma insulin ( e ) levels during an oral glucose tolerance test after 22 weeks of HFD. Corresponding area under the curve in iTBL/RβKO ( n = 8) and control ( n = 9) mice ( d , right). f , g Relative mRNA expression determined by qPCR in pancreatic islets of iTBL/RβKO and control mice of Tbl1x and Tbl1xr1 ( f ) and islet genes ( g ). Control mice Tbl1x , Tbl1xr1 , Ins1 , Ins2 , Nkx6.1 , Slc2a2 , Mafa , Pdx1 , Pax6 , Ucn3 : n = 9, control mice ChgA , Ngn3 , Ldha , Hk1 : n = 8, iTBL/RβKO mice Tbl1x , Ngn3 , Ldha , Hk1 : n = 7, iTBL/RβKO mice Tbl1xr1 , Ins1 , Ins2 , Slc2a2 , Mafa n = 6, iTBL/RβKO mice Nkx6.1 , Pdx1 , Pax6 , Ucn3 , ChgA : n = 5. h α/β-cell mass ratio of pancreatic islets from iTBL/RβKO ( n = 4) and control mice ( n = 4) on HFD, 24 weeks after knockout induction. i Representative immunofluorescent staining of insulin + (blue, β-cells) and glucagon + (red, α-cells) cells of paraffin-embedded pancreas from iTBL/RβKO and control mice on HFD, 24 weeks after knockout induction. Each point represents one mouse. Data are represented as mean ± SEM. The following statistical tests were applied: two-sided student’s t test ( d – Area under the curve, f – h ) and 2-way ANOVA with Šidák’s multiple comparison post hoc test ( b – d – time course, e ). Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: TBL1X/TBL1XR1 govern β-cell identity through a PAX6-containing gene regulatory network

doi: 10.1038/s41467-026-72077-5

Figure Lengend Snippet: a Scheme for the generation of an inducible β-cell-specific TBL1X and TBL1XR1 knockout. b Random fed blood glucose levels over time in iTBL/RβKO ( n = 9) and control ( n = 9) mice on HFD. c Total pancreas insulin content normalized to protein levels in iTBL/RβKO and control mice 4 and 11 weeks after tamoxifen administration. n = 3 for 4w control and iTBL/RβKO mice, n = 6 for 11w control mice, n = 4 for 11w iTBL/RβKO mice. d , e Blood glucose ( d ) and plasma insulin ( e ) levels during an oral glucose tolerance test after 22 weeks of HFD. Corresponding area under the curve in iTBL/RβKO ( n = 8) and control ( n = 9) mice ( d , right). f , g Relative mRNA expression determined by qPCR in pancreatic islets of iTBL/RβKO and control mice of Tbl1x and Tbl1xr1 ( f ) and islet genes ( g ). Control mice Tbl1x , Tbl1xr1 , Ins1 , Ins2 , Nkx6.1 , Slc2a2 , Mafa , Pdx1 , Pax6 , Ucn3 : n = 9, control mice ChgA , Ngn3 , Ldha , Hk1 : n = 8, iTBL/RβKO mice Tbl1x , Ngn3 , Ldha , Hk1 : n = 7, iTBL/RβKO mice Tbl1xr1 , Ins1 , Ins2 , Slc2a2 , Mafa n = 6, iTBL/RβKO mice Nkx6.1 , Pdx1 , Pax6 , Ucn3 , ChgA : n = 5. h α/β-cell mass ratio of pancreatic islets from iTBL/RβKO ( n = 4) and control mice ( n = 4) on HFD, 24 weeks after knockout induction. i Representative immunofluorescent staining of insulin + (blue, β-cells) and glucagon + (red, α-cells) cells of paraffin-embedded pancreas from iTBL/RβKO and control mice on HFD, 24 weeks after knockout induction. Each point represents one mouse. Data are represented as mean ± SEM. The following statistical tests were applied: two-sided student’s t test ( d – Area under the curve, f – h ) and 2-way ANOVA with Šidák’s multiple comparison post hoc test ( b – d – time course, e ). Source data are provided as a Source Data file.

Article Snippet: The following TaqMan probes were used: Tbp - Mm01277042_m1, Tbl1x - Mm01222202_m1, Tbl1xr1 - Mm01283877_m1, Ins1 - Mm01259683_g1, Ins2 - Mm00731595_gH, Nkx6.1 - Mm00454961_m1, Slc2a2 - Mm00454961_m1, Mafa - Mm00845206_s1, Pdx1 - Mm00435565_m1, Pax6 - Mm00443081_m1, Ucn3 - Mm00453206_s1, ChgA - Mm00514341_m1, Ngn3 - Mm00437606_s1, Ldha - Mm01612132_g1, Hk1 - Mm00439344_m1, TBP - Hs00427620_m1, TBL1X - Hs00959540_m1, TBL1XR1 - Hs00226564_m1.

Techniques: Knock-Out, Control, Clinical Proteomics, Expressing, Staining, Comparison

HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, LDHA , and SLC2A1 ( GLUT1 ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.

Journal: The Journal of Pathology

Article Title: Hypoxia‐inducible factor 1‐alpha does not regulate osteoclastogenesis but enhances bone resorption activity via prolyl‐4‐hydroxylase 2

doi: 10.1002/path.4906

Figure Lengend Snippet: HIF induction during osteoclast differentiation. (A) Western blot analysis of HIF‐1α protein expression in CD14+ monocytes treated with 25 ng/ml M‐CSF for 2–24 h versus the untreated normoxic control (Nx). Hx = hypoxia (2% O 2 , 24 h). (B) RT‐qPCR comparing HIF1A , HIF2A, LDHA , and SLC2A1 ( GLUT1 ) mRNA on days 3, 5, 7 and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01. (C) Western blot analysis of HIF‐1α, GLUT1, and LDHA protein on days 3, 5, and 9 of osteoclast differentiation. (D) Normalized HRE‐driven luciferase reporter luminescence on days 3, 5, 7, and 9 of osteoclast differentiation. * p < 0.05; ** p < 0.01.

Article Snippet: Primary antibodies were against HIF‐1α (clone 54, 1:1000; BD Biosciences, Oxford, UK), GLUT1 (ab14683, 1:2500; Abcam, Cambridge, UK), LDHA (NBP1‐48336, 1:2000; Novus Biologicals, Cambridge, UK), and β‐tubulin (clone TUB2.1, 1:2500; Sigma‐Aldrich, Dorset, UK).

Techniques: Western Blot, Expressing, Control, Quantitative RT-PCR, Luciferase

Figure 1. Cisplatin (CDDP) treatments decrease lactate dehydrogenase‑A (LDHA) expression. (A) CDDP treatments at 5, 10 and 50 µM in OECM‑1 and H‑1 cells decreased the level of LDHA expression. β‑actin served as a loading control. (B) Generation of the CDDP‑resistant cell line. OECM‑1 CDDP‑sensitive (Cis S) and CDDP‑resistant (Cis R) cells were treated at 10, 50 and 100 µM CDDP, followed by the measurement of cell viability. (C) Cis R clone number 1 (C1), and Cis R clone number 2 (C2) and the Cis R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represents the mean of three independent experiments and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.

Journal: Oncology letters

Article Title: Synergistic cytotoxicity of cisplatin and Taxol in overcoming Taxol resistance through the inhibition of LDHA in oral squamous cell carcinoma.

doi: 10.3892/ol.2015.2931

Figure Lengend Snippet: Figure 1. Cisplatin (CDDP) treatments decrease lactate dehydrogenase‑A (LDHA) expression. (A) CDDP treatments at 5, 10 and 50 µM in OECM‑1 and H‑1 cells decreased the level of LDHA expression. β‑actin served as a loading control. (B) Generation of the CDDP‑resistant cell line. OECM‑1 CDDP‑sensitive (Cis S) and CDDP‑resistant (Cis R) cells were treated at 10, 50 and 100 µM CDDP, followed by the measurement of cell viability. (C) Cis R clone number 1 (C1), and Cis R clone number 2 (C2) and the Cis R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represents the mean of three independent experiments and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.

Article Snippet: A vector containing wild-type LDHA was purchased from Origene (RC209378; Rockville, MD, USA).

Techniques: Expressing, Control, Cell Culture, Western Blot

Figure 2. Taxol‑resistant cells shows increased lactate dehydrogenase‑A (LDHA) expression. (A) Taxol treatments of 0.1, 1 and 10 µM in the OECM‑1 cells induced LDHA expression. β‑actin served as a loading control. (B) Generation of the Taxol‑resistant cell line. OECM‑1 Taxol‑sensitive (Tax S) and Taxol‑resistant (Tax R) cells were treated with 0.1, 1 and 20 µM Taxol, followed by the measurement of cell viability. (C) Tax R clone number 1 (C1), Tax R clone number 2 (C2) and the Tax R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represent the mean of three independent experiments, and the bars represent the standard error. *P<0.05 vs. control.

Journal: Oncology letters

Article Title: Synergistic cytotoxicity of cisplatin and Taxol in overcoming Taxol resistance through the inhibition of LDHA in oral squamous cell carcinoma.

doi: 10.3892/ol.2015.2931

Figure Lengend Snippet: Figure 2. Taxol‑resistant cells shows increased lactate dehydrogenase‑A (LDHA) expression. (A) Taxol treatments of 0.1, 1 and 10 µM in the OECM‑1 cells induced LDHA expression. β‑actin served as a loading control. (B) Generation of the Taxol‑resistant cell line. OECM‑1 Taxol‑sensitive (Tax S) and Taxol‑resistant (Tax R) cells were treated with 0.1, 1 and 20 µM Taxol, followed by the measurement of cell viability. (C) Tax R clone number 1 (C1), Tax R clone number 2 (C2) and the Tax R pool were cultured, and western blotting was performed to examine the LDHA expression levels. β‑actin served as a loading control. The data in the columns represent the mean of three independent experiments, and the bars represent the standard error. *P<0.05 vs. control.

Article Snippet: A vector containing wild-type LDHA was purchased from Origene (RC209378; Rockville, MD, USA).

Techniques: Expressing, Control, Cell Culture, Western Blot

Figure 3. Lactate dehydrogenase‑A (LDHA) plays reverse roles in response to Taxol and cisplatin (CDDP) treatments. (A) Knockdown of LHDA sensitized the OECM‑1 cells to Taxol treatment, but desensitized the OECM‑1 cells to the CDDP treatment. The OECM‑1 cells were transfected with small interfering (si)RNA for 48 h, then treated with CDDP at 10, 50 and 100 µM or Taxol at 0.1, 0.5 and 1 µM, followed by the measurement of cell viability. (B) Overexpression of LDHA sensitized the OECM‑1 cells to CDDP treatment, but desensitized the OECM‑1 cells to Taxol treatment. The OECM‑1 cells were transfected with overexpression vector containing wild‑type LDHA (V) for 48 h, then treated with CDDP at 5, 10 and 50 µM or Taxol at 0.1, 5 and 20 µM, followed by the measurement of cell viability. The columns represent the mean of three independent experiments, and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.

Journal: Oncology letters

Article Title: Synergistic cytotoxicity of cisplatin and Taxol in overcoming Taxol resistance through the inhibition of LDHA in oral squamous cell carcinoma.

doi: 10.3892/ol.2015.2931

Figure Lengend Snippet: Figure 3. Lactate dehydrogenase‑A (LDHA) plays reverse roles in response to Taxol and cisplatin (CDDP) treatments. (A) Knockdown of LHDA sensitized the OECM‑1 cells to Taxol treatment, but desensitized the OECM‑1 cells to the CDDP treatment. The OECM‑1 cells were transfected with small interfering (si)RNA for 48 h, then treated with CDDP at 10, 50 and 100 µM or Taxol at 0.1, 0.5 and 1 µM, followed by the measurement of cell viability. (B) Overexpression of LDHA sensitized the OECM‑1 cells to CDDP treatment, but desensitized the OECM‑1 cells to Taxol treatment. The OECM‑1 cells were transfected with overexpression vector containing wild‑type LDHA (V) for 48 h, then treated with CDDP at 5, 10 and 50 µM or Taxol at 0.1, 5 and 20 µM, followed by the measurement of cell viability. The columns represent the mean of three independent experiments, and the bars represent the standard error. *P<0.05 and **P<0.01 vs. control.

Article Snippet: A vector containing wild-type LDHA was purchased from Origene (RC209378; Rockville, MD, USA).

Techniques: Knockdown, Transfection, Over Expression, Plasmid Preparation, Control

Figure 4. Combination of Taxol and cisplatin (CDDP) shows synergistic effects on the Taxol‑resistant (Tax R) cells through the inhibition of lactate dehydro genase‑A (LDHA). (A) Tax R cells were treated with Taxol alone at 0.1, 1 and 20 µM, CDDP alone at 10 µM, 5‑FU alone at 500µM, Taxol plus CDDP or Taxol plus 5‑fluorouracil (FU), followed by the measurement of cell viability. (B) LDHA was downregulated in response to the treatment with the combination of Taxol and CDDP, but exhibited no change following treatment with the combination of Taxol and 5‑FU. (C) The overexpression of LDHA in the Taxol‑resistant (Tax R) cells resulted in acquired resistance to treatment with the combination of Taxol and CDDP. The cells were transfected with a vector containing wild‑type LDHA (V) for 48 h, followed by depletion of the medium and treatment with the drugs for 24 h. A cell viability assay was performed. Columns represent the mean of three independent experiments, and bars represent the standard error. *P<0.05 vs. control.

Journal: Oncology letters

Article Title: Synergistic cytotoxicity of cisplatin and Taxol in overcoming Taxol resistance through the inhibition of LDHA in oral squamous cell carcinoma.

doi: 10.3892/ol.2015.2931

Figure Lengend Snippet: Figure 4. Combination of Taxol and cisplatin (CDDP) shows synergistic effects on the Taxol‑resistant (Tax R) cells through the inhibition of lactate dehydro genase‑A (LDHA). (A) Tax R cells were treated with Taxol alone at 0.1, 1 and 20 µM, CDDP alone at 10 µM, 5‑FU alone at 500µM, Taxol plus CDDP or Taxol plus 5‑fluorouracil (FU), followed by the measurement of cell viability. (B) LDHA was downregulated in response to the treatment with the combination of Taxol and CDDP, but exhibited no change following treatment with the combination of Taxol and 5‑FU. (C) The overexpression of LDHA in the Taxol‑resistant (Tax R) cells resulted in acquired resistance to treatment with the combination of Taxol and CDDP. The cells were transfected with a vector containing wild‑type LDHA (V) for 48 h, followed by depletion of the medium and treatment with the drugs for 24 h. A cell viability assay was performed. Columns represent the mean of three independent experiments, and bars represent the standard error. *P<0.05 vs. control.

Article Snippet: A vector containing wild-type LDHA was purchased from Origene (RC209378; Rockville, MD, USA).

Techniques: Inhibition, Over Expression, Transfection, Plasmid Preparation, Viability Assay, Control

(A) Immunoblot showing overexpression of LDHA at 5 and 10 mg concentration of the LDHA plasmid in U87 cells, represented with LDHA and Myc tag LDHA. Quantification of the percentage of overexpression observed. (B) Cell viability of control, empty vector, and LDHA plasmid overexpression. Cell viability graphs of STP, TMZ, and GSK without overexpression of LDHA and with overexpression of LDHA. (C) Immunoblot representing LDHA knockdown by siLDHA. Quantification of the percentage decrease in LDHA expression. (D) Cell viability analysis of STP, TMZ, and GSK upon knockdown of LDHA. (E) Kinetic evaluation of LDHA enzyme activity assay with STP, and sodium oxamate. (F) Cell viability of SKNSH cells upon treatment with STP and Diazepam. n=3, *p<0.033, **p<0.002, ***p<0.001, one-way ANOVA Tukey test.

Journal: bioRxiv

Article Title: Mitochondrial Dysfunction and Senescence Accompany Glioblastoma Cell Death Triggered by a Putative Metabolic Inhibitor

doi: 10.1101/2025.09.08.674975

Figure Lengend Snippet: (A) Immunoblot showing overexpression of LDHA at 5 and 10 mg concentration of the LDHA plasmid in U87 cells, represented with LDHA and Myc tag LDHA. Quantification of the percentage of overexpression observed. (B) Cell viability of control, empty vector, and LDHA plasmid overexpression. Cell viability graphs of STP, TMZ, and GSK without overexpression of LDHA and with overexpression of LDHA. (C) Immunoblot representing LDHA knockdown by siLDHA. Quantification of the percentage decrease in LDHA expression. (D) Cell viability analysis of STP, TMZ, and GSK upon knockdown of LDHA. (E) Kinetic evaluation of LDHA enzyme activity assay with STP, and sodium oxamate. (F) Cell viability of SKNSH cells upon treatment with STP and Diazepam. n=3, *p<0.033, **p<0.002, ***p<0.001, one-way ANOVA Tukey test.

Article Snippet: U87 cell line was purchased from ATCC (USA), fetal bovine serum (FBS) (Atlanta Bio, USA), Dulbecco’s modified Eagle medium (DMEM), PSA, and Trypsin (Corning, USA), stiripentol and temozolomide (Fisher, USA), GSK2837807 sodium oxamate (Sigma, USA), siLDHA and Lipofectamine RNAimax (Life technologies, USA), LDHA plasmid (Origene, USA), Transit LT-1 (Mirrus, USA), Opti-MEM (Gibco, USA), BCA (Thermoscientific, USA), Direct-Zol RNA extraction kit (Zymo research, USA), CMH 2 DCFDA and CMXROS (Invitrogen, USA), primary antibodies β-actin, ALDHA13, AOX1, CPA4, TXNIP, KYNU, (Proteintech, USA), LC3 (Sigma) secondary antibodies anti-mouse, anti-rabbit, and senescence kit (Cell signaling, USA).

Techniques: Western Blot, Over Expression, Concentration Assay, Plasmid Preparation, Control, Knockdown, Expressing, Enzyme Activity Assay