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anti rabbit peroxiredoxin 6 prdx6 (Proteintech)

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Proteintech anti rabbit peroxiredoxin 6 prdx6

The proteins that interact with ALDH2 are enriched for mass spectrometry, and the results show that there is an interaction between PRDX1, 2, 4, 6, and ALDH2 ( A ). We separated the cytoplasm and mitochondrial proteins of SH-SY5Y cells, and then detected the levels of ALDH2 and <t>PRDX6</t> proteins in these two parts of the protein. We choose GAPDH as the cytoplasmic loading control and VDAC1 as the mitochondrial loading control ( B ). SH-SY5Y cells were transfected with NC, ALDH2, and rs671-ALDH2 overexpression plasmids for 48h, their total protein lysate was used for CO-IP experiments, and the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( C ). The WT, ALDH2 KO, and rs671 mice brain tissues were lysed for the CO-IP experiment; the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( D ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to the cell lysate separately or at the same time, after incubating at 4 °C for 6 h CO-IP experiment was conducted. Group IgG is a negative control ( E , F) Fluorescence confocal microscope observes the co-localization of ALDH2 (red) and PRDX6 (green). NC, ALDH2, or shPRDX6 plasmids were transfected into the SH-SY5Y cells for 24 h and then treated with 3 μM RSL-3 or 2.5 mM MPP + for 24 h. Cell viability changes were detected by CCK8 assay ( G ), and GSH and Lipid peroxide products (LOOH) were detected by the GSH assay kit or Flow cytometer ( H , I ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Anti Rabbit Peroxiredoxin 6 Prdx6, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+prdx6/pmc12689773-267-35-41?v=Proteintech
Average 95 stars, based on 45 article reviews

anti rabbit peroxiredoxin 6 prdx6 - by Bioz Stars, 2026-08

95/100 stars

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1) Product Images from "ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson’s disease"

Article Title: ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson’s disease

Journal: NPJ Parkinson's Disease

doi: 10.1038/s41531-025-01155-0

Figure Legend Snippet: The proteins that interact with ALDH2 are enriched for mass spectrometry, and the results show that there is an interaction between PRDX1, 2, 4, 6, and ALDH2 ( A ). We separated the cytoplasm and mitochondrial proteins of SH-SY5Y cells, and then detected the levels of ALDH2 and PRDX6 proteins in these two parts of the protein. We choose GAPDH as the cytoplasmic loading control and VDAC1 as the mitochondrial loading control ( B ). SH-SY5Y cells were transfected with NC, ALDH2, and rs671-ALDH2 overexpression plasmids for 48h, their total protein lysate was used for CO-IP experiments, and the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( C ). The WT, ALDH2 KO, and rs671 mice brain tissues were lysed for the CO-IP experiment; the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( D ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to the cell lysate separately or at the same time, after incubating at 4 °C for 6 h CO-IP experiment was conducted. Group IgG is a negative control ( E , F) Fluorescence confocal microscope observes the co-localization of ALDH2 (red) and PRDX6 (green). NC, ALDH2, or shPRDX6 plasmids were transfected into the SH-SY5Y cells for 24 h and then treated with 3 μM RSL-3 or 2.5 mM MPP + for 24 h. Cell viability changes were detected by CCK8 assay ( G ), and GSH and Lipid peroxide products (LOOH) were detected by the GSH assay kit or Flow cytometer ( H , I ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Techniques Used: Mass Spectrometry, Control, Transfection, Over Expression, Co-Immunoprecipitation Assay, Concentration Assay, Negative Control, Recombinant, Fluorescence, Microscopy, CCK-8 Assay, GSH Assay, Flow Cytometry

NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Total GPx enzyme activity was detected by a kit ( A , B ). NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Selenium-containing GPx activity was detected by a kit ( C , D ). After infection for 48 h, SH-SY5Y cells were treated with 2.5 mM MPP + for 24 h. Selenium-free GPx enzyme activity was detected by a kit ( E , F ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to 100 μl cell lysate separately or at the same time, incubated at 25 °C for 1 h, then detect the GPx enzyme activity of the two samples ( G ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Figure Legend Snippet: NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Total GPx enzyme activity was detected by a kit ( A , B ). NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Selenium-containing GPx activity was detected by a kit ( C , D ). After infection for 48 h, SH-SY5Y cells were treated with 2.5 mM MPP + for 24 h. Selenium-free GPx enzyme activity was detected by a kit ( E , F ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to 100 μl cell lysate separately or at the same time, incubated at 25 °C for 1 h, then detect the GPx enzyme activity of the two samples ( G ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Techniques Used: Mutagenesis, Transfection, Activity Assay, Infection, Recombinant, Incubation

We found that ALDH2 KO mice were more sensitive to the neurotoxin MPTP, and the behavioral disorder in ALDH2 KO mice was more severe than that in WT mice after MPTP treatment, in which TH-positive neurons in the SN were significantly reduced. Further research found that after MPTP treatment, the behavioral disorder and TH-positive neuron loss in ALDH2 rs671 site mutant mice were more serious than in WT mice, suggesting that the rs671 site mutation may be involved in the pathogenesis of PD. In our experiments, we found that ferroptosis-related phenotypes, such as decreased GSH and increased lipid peroxides, were altered in PD in both in vivo and in vitro models, and that the expression of ALDH2 could affect the sensitivity of SH-SY5Y cells to ferroptosis agonists. Further, our research showed that ALDH2 interacts with PRDX6 and affects its enzymatic activity, thereby regulating ferroptosis. In addition, the mutation at rs671 in the ALDH2 gene weakens its binding to PRDX6 and reduces the effect of ALDH2 on PRDX6 enzyme activity. These results support the hypothesis that impaired detoxification of ALDH2 may be important in the pathophysiology of PD and suggest that ALDH2 may affect the sensitivity of dopaminergic cells to ferroptosis by regulating the enzyme activity of PRDX6.

Figure Legend Snippet: We found that ALDH2 KO mice were more sensitive to the neurotoxin MPTP, and the behavioral disorder in ALDH2 KO mice was more severe than that in WT mice after MPTP treatment, in which TH-positive neurons in the SN were significantly reduced. Further research found that after MPTP treatment, the behavioral disorder and TH-positive neuron loss in ALDH2 rs671 site mutant mice were more serious than in WT mice, suggesting that the rs671 site mutation may be involved in the pathogenesis of PD. In our experiments, we found that ferroptosis-related phenotypes, such as decreased GSH and increased lipid peroxides, were altered in PD in both in vivo and in vitro models, and that the expression of ALDH2 could affect the sensitivity of SH-SY5Y cells to ferroptosis agonists. Further, our research showed that ALDH2 interacts with PRDX6 and affects its enzymatic activity, thereby regulating ferroptosis. In addition, the mutation at rs671 in the ALDH2 gene weakens its binding to PRDX6 and reduces the effect of ALDH2 on PRDX6 enzyme activity. These results support the hypothesis that impaired detoxification of ALDH2 may be important in the pathophysiology of PD and suggest that ALDH2 may affect the sensitivity of dopaminergic cells to ferroptosis by regulating the enzyme activity of PRDX6.

Techniques Used: Mutagenesis, In Vivo, In Vitro, Expressing, Activity Assay, Binding Assay

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Journal: NPJ Parkinson's Disease

Article Title: ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson’s disease

doi: 10.1038/s41531-025-01155-0

Figure Lengend Snippet: The proteins that interact with ALDH2 are enriched for mass spectrometry, and the results show that there is an interaction between PRDX1, 2, 4, 6, and ALDH2 ( A ). We separated the cytoplasm and mitochondrial proteins of SH-SY5Y cells, and then detected the levels of ALDH2 and PRDX6 proteins in these two parts of the protein. We choose GAPDH as the cytoplasmic loading control and VDAC1 as the mitochondrial loading control ( B ). SH-SY5Y cells were transfected with NC, ALDH2, and rs671-ALDH2 overexpression plasmids for 48h, their total protein lysate was used for CO-IP experiments, and the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( C ). The WT, ALDH2 KO, and rs671 mice brain tissues were lysed for the CO-IP experiment; the concentration of each antibody added is 0.2 μg/ml. Group IgG was a negative control ( D ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to the cell lysate separately or at the same time, after incubating at 4 °C for 6 h CO-IP experiment was conducted. Group IgG is a negative control ( E , F) Fluorescence confocal microscope observes the co-localization of ALDH2 (red) and PRDX6 (green). NC, ALDH2, or shPRDX6 plasmids were transfected into the SH-SY5Y cells for 24 h and then treated with 3 μM RSL-3 or 2.5 mM MPP + for 24 h. Cell viability changes were detected by CCK8 assay ( G ), and GSH and Lipid peroxide products (LOOH) were detected by the GSH assay kit or Flow cytometer ( H , I ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Article Snippet: The membranes were blocked for 1 h at room temperature with 5% nonfat milk in tris buffered saline Tween-20 (TBST), then incubated overnight at 4 °C with specific primary antibodies: anti-rabbit ALDH2 (1:1000, 15310-1-AP, Proteintech), anti-rabbit peroxiredoxin 6 (PRDX6) (1:1000, 13585-1-AP, Proteintech), anti-rabbit VDAC1 (1:1000, 55259-1-AP, Proteintech), anti-mouse glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (1:1000, 60004-1-lg, Proteintech), and anti-mouse tyrosine hydroxylase (TH) (1:1000, T2928, Sigma).

Techniques: Mass Spectrometry, Control, Transfection, Over Expression, Co-Immunoprecipitation Assay, Concentration Assay, Negative Control, Recombinant, Fluorescence, Microscopy, CCK-8 Assay, GSH Assay, Flow Cytometry

Journal: NPJ Parkinson's Disease

Article Title: ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson’s disease

doi: 10.1038/s41531-025-01155-0

Figure Lengend Snippet: NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Total GPx enzyme activity was detected by a kit ( A , B ). NC, ALDH2, shPRDX6, or ALDH2 rs671 mutant plasmids were transfected into the SH-SY5Y cells for 48 h, and then the treated cells with 2.5 mM MPP + for 24 h. Selenium-containing GPx activity was detected by a kit ( C , D ). After infection for 48 h, SH-SY5Y cells were treated with 2.5 mM MPP + for 24 h. Selenium-free GPx enzyme activity was detected by a kit ( E , F ). Add 1 μl each of recombinant human ALDH2 protein and recombinant human PRDX6 protein to 100 μl cell lysate separately or at the same time, incubated at 25 °C for 1 h, then detect the GPx enzyme activity of the two samples ( G ). Data are expressed as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3.

Techniques: Mutagenesis, Transfection, Activity Assay, Infection, Recombinant, Incubation

Journal: NPJ Parkinson's Disease

Article Title: ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson’s disease

doi: 10.1038/s41531-025-01155-0

Figure Lengend Snippet: We found that ALDH2 KO mice were more sensitive to the neurotoxin MPTP, and the behavioral disorder in ALDH2 KO mice was more severe than that in WT mice after MPTP treatment, in which TH-positive neurons in the SN were significantly reduced. Further research found that after MPTP treatment, the behavioral disorder and TH-positive neuron loss in ALDH2 rs671 site mutant mice were more serious than in WT mice, suggesting that the rs671 site mutation may be involved in the pathogenesis of PD. In our experiments, we found that ferroptosis-related phenotypes, such as decreased GSH and increased lipid peroxides, were altered in PD in both in vivo and in vitro models, and that the expression of ALDH2 could affect the sensitivity of SH-SY5Y cells to ferroptosis agonists. Further, our research showed that ALDH2 interacts with PRDX6 and affects its enzymatic activity, thereby regulating ferroptosis. In addition, the mutation at rs671 in the ALDH2 gene weakens its binding to PRDX6 and reduces the effect of ALDH2 on PRDX6 enzyme activity. These results support the hypothesis that impaired detoxification of ALDH2 may be important in the pathophysiology of PD and suggest that ALDH2 may affect the sensitivity of dopaminergic cells to ferroptosis by regulating the enzyme activity of PRDX6.

Techniques: Mutagenesis, In Vivo, In Vitro, Expressing, Activity Assay, Binding Assay

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