Standout Papers

HIF-1α, STAT3, CBP/p300 and Ref-1/APE are components of a transcriptional complex that regulate... 2005 2026 2012 2019 320
  1. HIF-1α, STAT3, CBP/p300 and Ref-1/APE are components of a transcriptional complex that regulates Src-dependent hypoxia-induced expression of VEGF in pancreatic and prostate carcinomas (2005)
    Michael J. Gray, Jing Zhang et al. Oncogene

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Works of Michael J. Gray being referenced

Overexpression of neuropilin-1 promotes constitutive MAPK signalling and chemoresistance in pancreatic cancer cells
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Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells
2006
HIF-1α, STAT3, CBP/p300 and Ref-1/APE are components of a transcriptional complex that regulates Src-dependent hypoxia-induced expression of VEGF in pancreatic and prostate carcinomas
2005 StandoutNobel
Macrophage depletion alters the blood–nerve barrier without affecting Schwann cell function after neural injury
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Functional significance of vascular endothelial growth factor receptors on gastrointestinal cancer cells
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Induction of arginase I transcription by IL-4 requires a composite DNA response element for STAT6 and C/EBPβ
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Polyphosphate Is a Primordial Chaperone
2014
Vascular endothelial growth factor receptor‐1 promotes migration and invasion in pancreatic carcinoma cell lines
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Vascular Endothelial Growth Factor Receptor-1 Activation Mediates Epithelial to Mesenchymal Transition in Human Pancreatic Carcinoma Cells
2006
Neuropilin-1 Suppresses Tumorigenic Properties in a Human Pancreatic Adenocarcinoma Cell Line Lacking Neuropilin-1 Coreceptors
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Single-enzyme conversion of FMNH 2 to 5,6-dimethylbenzimidazole, the lower ligand of B 12
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Endoglin (CD105): A Marker of Tumor Vasculature and Potential Target for Therapy
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The Development and Characterization of a Human Midgut Carcinoid Cell Line
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Chronic Oxaliplatin Resistance Induces Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cell Lines
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Chemoresistant Colorectal Cancer Cells, the Cancer Stem Cell Phenotype, and Increased Sensitivity to Insulin-like Growth Factor-I Receptor Inhibition
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