Dilair Baban
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View article: Pigment Epithelium Derived Factor Drives Melanocyte Proliferation and Migration in Neurofibromatosis Café Au Lait Macules
Pigment Epithelium Derived Factor Drives Melanocyte Proliferation and Migration in Neurofibromatosis Café Au Lait Macules Open
Background RASopathies, which include neurofibromatosis type 1 (NF1), are defined by Ras/mitogen-activated protein kinase (Ras/MAPK) pathway activation. They represent a group of clinically related disorders often characterised by multiple…
View article: Supplementary Figure 2 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 2 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S2. (A) Kaplan-Meier analysis of overall survival of 440 colon adenocarcinoma patients TGCA cohort. Patient group with highest quartile showed a reduced five-year survival. (B) Heatmap illustrating the correlative gene expression profile o…
View article: Supplementary Figure 8 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 8 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S8. Hydrophilic metabolites detection and identification performed by LC/MS QTOF nanoflow using AMRT comparison.
View article: Supplementary Figure 1 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 1 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S1. Blocking O-GlcNAcylation in vivo by inducing shOGT or alloxan treatment qualitatively reduces EZH2 immunoreactivity after irradiation.
View article: Authorship Change Form from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Authorship Change Form from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S8. WTN, KON, WTH, and KOH HCT116 cell proliferation after 5 days in two O2 conditions,21% and 1% for cells knocked down for GTR3, GTR14 , and HIF2α
View article: Supplementary Figure 4 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 4 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S4. Hypoxic regulation of glucose transporters and creatine kinases validation by PCR and western blot analysis.
View article: Supplementary Figure 6 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 6 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S6. Phosphocreatine/Creatine ratio per cell in WTN, KON, WTH, and KOH.
View article: Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
Hypoxia-inducible factor 1α is a key regulator of the hypoxia response in normal and cancer tissues. It is well recognized to regulate glycolysis and is a target for therapy. However, how tumor cells adapt to grow in the absence of HIF1α i…
View article: Supplementary Figure 5 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 5 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S5. Statistical significance for mRNA PCR data.
View article: Supplemetary Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplemetary Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
Supplementary materials and methods
View article: Supplementary Figure 4 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 4 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S4. Hypoxic regulation of glucose transporters and creatine kinases validation by PCR and western blot analysis.
View article: Supplementary Figure 7 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 7 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S7. WTN, KON, WTH, and KOH HCT116 cell proliferation after 5 days in two O2 conditions, 21% and 1% for cells knocked down for GTR3, GTR14, and HIF2α.
View article: Supplementary Figure 3 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 3 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S3. HIF1α and hypoxia-dependent effects on transcription and protein levels.
View article: Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
Hypoxia-inducible factor 1α is a key regulator of the hypoxia response in normal and cancer tissues. It is well recognized to regulate glycolysis and is a target for therapy. However, how tumor cells adapt to grow in the absence of HIF1α i…
View article: Supplementary Figure 6 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 6 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S6. Phosphocreatine/Creatine ratio per cell in WTN, KON, WTH, and KOH.
View article: Supplementary Figure 7 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 7 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S7. WTN, KON, WTH, and KOH HCT116 cell proliferation after 5 days in two O2 conditions, 21% and 1% for cells knocked down for GTR3, GTR14, and HIF2α.
View article: Supplemetary Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplemetary Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
Supplementary materials and methods
View article: Supplementary Figure 1 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 1 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S1. Blocking O-GlcNAcylation in vivo by inducing shOGT or alloxan treatment qualitatively reduces EZH2 immunoreactivity after irradiation.
View article: Supplementary Figure 8 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 8 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S8. Hydrophilic metabolites detection and identification performed by LC/MS QTOF nanoflow using AMRT comparison.
View article: Authorship Change Form from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Authorship Change Form from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S8. WTN, KON, WTH, and KOH HCT116 cell proliferation after 5 days in two O2 conditions,21% and 1% for cells knocked down for GTR3, GTR14 , and HIF2α
View article: Supplementary Figure 2 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 2 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S2. (A) Kaplan-Meier analysis of overall survival of 440 colon adenocarcinoma patients TGCA cohort. Patient group with highest quartile showed a reduced five-year survival. (B) Heatmap illustrating the correlative gene expression profile o…
View article: Supplementary Figure 3 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 3 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S3. HIF1α and hypoxia-dependent effects on transcription and protein levels.
View article: Supplementary Figure 5 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism
Supplementary Figure 5 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism Open
S5. Statistical significance for mRNA PCR data.
View article: Supplementary Methods, Figure Legends 1-6, Tables 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
Supplementary Methods, Figure Legends 1-6, Tables 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth Open
Supplementary Methods, Figure Legends 1-6, Tables 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
View article: Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis Open
Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
View article: Data from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
Data from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth Open
Estrogen receptor α (ERα) plays an important role in breast cancer. Upregulation of HIF-1α in ERα-positive cancers suggests that HIF-1α may cooperate with ERα to promote breast cancer progression and consequently affect breast cancer treat…
View article: Data from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
Data from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth Open
Estrogen receptor α (ERα) plays an important role in breast cancer. Upregulation of HIF-1α in ERα-positive cancers suggests that HIF-1α may cooperate with ERα to promote breast cancer progression and consequently affect breast cancer treat…
View article: Supplementary Figures 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
Supplementary Figures 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth Open
Supplementary Figures 1-6 from The Histone Demethylase JMJD2B Is Regulated by Estrogen Receptor α and Hypoxia, and Is a Key Mediator of Estrogen Induced Growth
View article: Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis Open
Supplementary Figures 1-8 from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
View article: Data from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
Data from A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis Open
Invasion of lymphatic vessels is a key step in the metastasis of primary tumors to draining lymph nodes. Although the process is enhanced by tumor lymphangiogenesis, it is unclear whether this is a consequence of increased lymphatic vessel…