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Proteintech anti ldha
Anti Ldha, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 227 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti ldha - by Bioz Stars, 2026-05
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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.
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<t>LDHA</t> overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis <t>of</t> <t>caspase-3,</t> Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .
Ldha, supplied by Cell Signaling Technology Inc, 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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<t>LDHA</t> overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis <t>of</t> <t>caspase-3,</t> Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .
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<t>LDHA</t> overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis <t>of</t> <t>caspase-3,</t> Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .
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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<t>LDHA</t> overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis <t>of</t> <t>caspase-3,</t> Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .
Anti Ldha, supplied by Cell Signaling Technology Inc, 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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<t>LDHA</t> overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis <t>of</t> <t>caspase-3,</t> Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .
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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

LDHA overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis of caspase-3, Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .

Journal: Molecular Medicine Reports

Article Title: LDHA protects vascular endothelial cells from oxidative stress-induced mitochondrial damage via HIF-1α activation and glycolytic reprogramming

doi: 10.3892/mmr.2026.13851

Figure Lengend Snippet: LDHA overexpression mitigates apoptosis and mitochondrial damage in OGD/R-treated VECs. (A) Reverse transcription-quantitative polymerase chain reaction analysis of LDHA mRNA in VECs transfected with vector or over-LDHA. (B) Representative western blot analysis of LDHA with β-actin as loading control. (C) Semi-quantification of LDHA protein expression relative to β-actin. (D) Transmission electron microscopy images of VECs at ×2,500 magnification showing mitochondrial morphology. Red arrows indicate mitochondria (swollen and with disrupted cristae under OGD/R conditions). Scale bar: 500 nm. (E) Western blot analysis of caspase-3, Cyt-c and Mcl-1 in VECs from the indicated groups; β-actin was used as the loading control. (F) Densitometric semi-quantification of relative protein expression normalized to β-actin for caspase-3, Cyt-c and Mcl-1. (G) Flow cytometric analysis of the effects of LDHA overexpression on apoptosis levels in VECs subjected to H 2 O 2 (OGD/R) treatment. Data are presented as the mean ± SD of three independent experiments. *P<0.05 vs. vector or as indicated. H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; WB, western blotting; PI, propidium iodide; FITC, fluorescein isothiocyanate; Cyt-c, cytochrome c .

Article Snippet: Subsequently, the membranes were incubated overnight at 4°C with primary antibodies against the following proteins: LDHA (1:1,000; cat. no. 2012; Cell Signaling Technology, Inc.), caspase-3 (1:5,000; cat. no. ab32351; Abcam), caspase-9 (1:2,000; cat. no. ab202068; Abcam), caspase-8 (1:1,000; cat. no. ab32397; Abcam), cytochrome c (Cyt-c; 1:5,000; cat. no. ab133504; Abcam), Mcl-1 (1:1,000; cat. no. ab32087; Abcam), HIF-1α (1:1,000; cat. no. ab51608; Abcam), sodium-calcium exchanger 1 (NCX1; 1:1,000; cat. no. ab177952; Abcam), sodium-proton exchanger 1 (NHE1; 1:1,000; cat. no. ab67313; Abcam) and monocarboxylate transporter 4 (MCT4; 1:1,000; cat. no. ab308528; Abcam), with β-actin (1:1,000; cat. no. ab8227; Abcam) used as an internal loading control for whole-cell and cytoplasmic proteins, and Lamin B1 (1:20,000; cat. no. 12987–1-AP; Wuhan Sanying Biotechnology) used as a nuclear loading control.

Techniques: Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Transfection, Plasmid Preparation, Western Blot, Control, Expressing, Transmission Assay, Electron Microscopy

LDHA protects against oxidative stress-induced mitochondrial damage through glycolytic reprogramming in VECs. (A) Representative WB images of caspase-3, Cyt-c and Mcl-1 protein expression in VECs treated with 0.5 mM H 2 O 2 (OGD/R) and overexpressing LDHA, with or without 2-DG. Semi-quantification of (B) caspase-3, (C) Cyt-c and (D) Mcl-1 protein levels normalized to internal controls. Measurement of (E) ROS, (F) MDA and (G) GSH levels in each group. Data are presented as the mean ± SD from three independent experiments. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001 . H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; 2-DG, 2-deoxy-D-glucose; WB, western blotting; ROS, reactive oxygen species; MDA, malondialdehyde; GSH, glutathione; Cyt-c, cytochrome c .

Journal: Molecular Medicine Reports

Article Title: LDHA protects vascular endothelial cells from oxidative stress-induced mitochondrial damage via HIF-1α activation and glycolytic reprogramming

doi: 10.3892/mmr.2026.13851

Figure Lengend Snippet: LDHA protects against oxidative stress-induced mitochondrial damage through glycolytic reprogramming in VECs. (A) Representative WB images of caspase-3, Cyt-c and Mcl-1 protein expression in VECs treated with 0.5 mM H 2 O 2 (OGD/R) and overexpressing LDHA, with or without 2-DG. Semi-quantification of (B) caspase-3, (C) Cyt-c and (D) Mcl-1 protein levels normalized to internal controls. Measurement of (E) ROS, (F) MDA and (G) GSH levels in each group. Data are presented as the mean ± SD from three independent experiments. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001 . H 2 O 2 , hydrogen peroxide; OGD/R, oxygen-glucose deprivation/reperfusion; VECs, vascular endothelial cells; LDHA, lactate dehydrogenase A; 2-DG, 2-deoxy-D-glucose; WB, western blotting; ROS, reactive oxygen species; MDA, malondialdehyde; GSH, glutathione; Cyt-c, cytochrome c .

Article Snippet: Subsequently, the membranes were incubated overnight at 4°C with primary antibodies against the following proteins: LDHA (1:1,000; cat. no. 2012; Cell Signaling Technology, Inc.), caspase-3 (1:5,000; cat. no. ab32351; Abcam), caspase-9 (1:2,000; cat. no. ab202068; Abcam), caspase-8 (1:1,000; cat. no. ab32397; Abcam), cytochrome c (Cyt-c; 1:5,000; cat. no. ab133504; Abcam), Mcl-1 (1:1,000; cat. no. ab32087; Abcam), HIF-1α (1:1,000; cat. no. ab51608; Abcam), sodium-calcium exchanger 1 (NCX1; 1:1,000; cat. no. ab177952; Abcam), sodium-proton exchanger 1 (NHE1; 1:1,000; cat. no. ab67313; Abcam) and monocarboxylate transporter 4 (MCT4; 1:1,000; cat. no. ab308528; Abcam), with β-actin (1:1,000; cat. no. ab8227; Abcam) used as an internal loading control for whole-cell and cytoplasmic proteins, and Lamin B1 (1:20,000; cat. no. 12987–1-AP; Wuhan Sanying Biotechnology) used as a nuclear loading control.

Techniques: Expressing, Western Blot