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View article: Author Correction: LILRB3 genetic variation is associated with kidney transplant failure in African American recipients
Author Correction: LILRB3 genetic variation is associated with kidney transplant failure in African American recipients Open
View article: Transsulfuration pathway activation attenuates oxidative stress and ferroptosis in sickle primary erythroblasts and transgenic mice
Transsulfuration pathway activation attenuates oxidative stress and ferroptosis in sickle primary erythroblasts and transgenic mice Open
The transsulfuration (TSS) pathway is an alternative source of cysteine for glutathione synthesis. Little of the TSS pathway in antioxidant capacity in sickle cell disease (SCD) is known. Here, we evaluate the effects of TSS pathway activa…
View article: Simvastatin-Mediated Nrf2 Activation Induces Fetal Hemoglobin and Antioxidant Enzyme Expression to Ameliorate the Phenotype of Sickle Cell Disease
Simvastatin-Mediated Nrf2 Activation Induces Fetal Hemoglobin and Antioxidant Enzyme Expression to Ameliorate the Phenotype of Sickle Cell Disease Open
Sickle cell disease (SCD) is a pathophysiological condition of chronic hemolysis, oxidative stress, and elevated inflammation. The transcription factor Nrf2 is a master regulator of oxidative stress. Here, we report that the FDA-approved o…
View article: Genetic polymorphisms of Leukocyte Immunoglobulin-Like Receptor B3 (<i>LILRB3</i>) gene in African American kidney transplant recipients are associated with post-transplant graft failure
Genetic polymorphisms of Leukocyte Immunoglobulin-Like Receptor B3 (<i>LILRB3</i>) gene in African American kidney transplant recipients are associated with post-transplant graft failure Open
Background African American (AA) kidney transplant recipients exhibit a higher rate of graft loss compared to other racial and ethnic populations, highlighting the need to identify causative factors underlying this disparity. Method We ana…
View article: Simvastatin-Mediated Nrf2 Activation Induces Fetal Hemoglobin and Antioxidant Enzyme Expression to Ameliorate the Phenotype of Sickle Cell Disease
Simvastatin-Mediated Nrf2 Activation Induces Fetal Hemoglobin and Antioxidant Enzyme Expression to Ameliorate the Phenotype of Sickle Cell Disease Open
Sickle cell disease (SCD) is a pathophysiological condition of chronic hemolysis, oxidative stress, and elevated inflammation. The transcription factor Nrf2 is a master regulator of oxidative stress. Here we reported that the FDA-approved,…
View article: A large-scale retrospective study enabled deep-learning based pathological assessment of frozen procurement kidney biopsies to predict graft loss and guide organ utilization
A large-scale retrospective study enabled deep-learning based pathological assessment of frozen procurement kidney biopsies to predict graft loss and guide organ utilization Open
View article: Supplementary Figure 2 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 2 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S2. Nrf2 ablation affects gene expression in mouse liver tumors.
View article: Supplementary Figure 4 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 4 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplementary Figure 4. NRF2 silencing shows no effect on histone acetylation or acetyl-CoA.
View article: Supplementary Figure 6 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 6 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S6. A glucose dependency of NRF2 regulation in HepG2 cells.
View article: Supplementary Figure 3 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 3 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S3. Nrf2 ablation shows no effect on the levels of acetyl-CoA or CoASH in tumor adjacent liver tissues.
View article: Supplementary Figure 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S1. RF2 promotes hepatocarcinogenesis.
View article: Supplemental material and methods from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplemental material and methods from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplemental material and methods
View article: Supplementary Figure 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S1. RF2 promotes hepatocarcinogenesis.
View article: Supplementary Figure 7 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 7 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S7. Nrf2 suppression decreases liver tumor progression.
View article: Supplementary Figure 4 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 4 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplementary Figure 4. NRF2 silencing shows no effect on histone acetylation or acetyl-CoA.
View article: Supplementary Figure 5 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 5 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S5. Hypoxia shows no contribution to the NRF2 regulated histone acetylation.
View article: Supplementary Figure 3 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 3 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S3. Nrf2 ablation shows no effect on the levels of acetyl-CoA or CoASH in tumor adjacent liver tissues.
View article: Supplemental material and methods from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplemental material and methods from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplemental material and methods
View article: Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S8. GCK and ALDOA gene expression in glucose-deprived shNRF2 HepG2 cells after energy-refeeding.
View article: Supplementary Figure 7 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 7 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S7. Nrf2 suppression decreases liver tumor progression.
View article: Data from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Data from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Correlations between the oxidative stress response and metabolic reprogramming have been observed during malignant tumor formation; however, the detailed mechanism remains elusive. The transcription factor Nrf2, a master regulator of the o…
View article: Supplementary Figure 5 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 5 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S5. Hypoxia shows no contribution to the NRF2 regulated histone acetylation.
View article: Supplemental Table 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplemental Table 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplemental Table 1. DNA Oligos
View article: Supplementary Figure 2 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 2 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S2. Nrf2 ablation affects gene expression in mouse liver tumors.
View article: Supplementary Figure 9 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 9 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S9. MYC silencing reduced the expression of glycolysis genes in HepG2 cells.
View article: Supplemental Table 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplemental Table 1 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
Supplemental Table 1. DNA Oligos
View article: Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S8. GCK and ALDOA gene expression in glucose-deprived shNRF2 HepG2 cells after energy-refeeding.
View article: Supplementary Figure 6 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 6 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S6. A glucose dependency of NRF2 regulation in HepG2 cells.
View article: Supplementary Figure 9 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 9 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–Mediated Metabolic and Epigenetic Regulatory Networks Open
S9. MYC silencing reduced the expression of glycolysis genes in HepG2 cells.
View article: Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks
Supplementary Figure 8 from Nrf2 Drives Hepatocellular Carcinoma Progression through Acetyl-CoA–mediated Metabolic and Epigenetic Regulatory Networks Open
S8. GCK and ALDOA gene expression in glucose-deprived shNRF2 HepG2 cells after energy-refeeding.