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Badarch Uranchimeg

Researcher at Science Applications International Corporation

Publications -  17
Citations -  2544

Badarch Uranchimeg is an academic researcher from Science Applications International Corporation. The author has contributed to research in topics: Angiogenesis & Receptor. The author has an hindex of 14, co-authored 17 publications receiving 2430 citations.

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Journal ArticleDOI

Regulation of the chemokine receptor CXCR4 by hypoxia.

TL;DR: It is described that oxygen availability is a determinant parameter in the setting of chemotactic responsiveness to stromal-derived factor 1 (CXCL12), and the Hyp–Hyp-inducible factor 1 α–CXCR4 pathway may regulate trafficking in and out of hypoxic tissue microenvironments.
Journal Article

Identification of Small Molecule Inhibitors of Hypoxia-inducible Factor 1 Transcriptional Activation Pathway

TL;DR: The luciferase-based high-throughput screen is a feasible tool for the identification of small molecule inhibitors of HIF-1 transcriptional activation and the results suggest that altered Topo-I function may be associated with repression of Hif-1-dependent induction of gene expression.
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Topoisomerase I-mediated inhibition of hypoxia-inducible factor 1: mechanism and therapeutic implications.

TL;DR: It is demonstrated that TPT does not affect Hif-1α protein half-life or mRNA accumulation but inhibits its translation, and the existence of a novel pathway connecting Top 1-dependent signaling events and the regulation of HIF-1 α protein expression and function is demonstrated.
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Hypoxic induction of an HIF-1α–dependent bFGF autocrine loop drives angiogenesis in human endothelial cells

TL;DR: The results uncover the existence of an HIF-1alpha-bFGF amplification pathway that mediates survival and sprouting of endothelial cells under hypoxic conditions.
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Schedule-dependent Inhibition of Hypoxia-inducible Factor-1α Protein Accumulation, Angiogenesis, and Tumor Growth by Topotecan in U251-HRE Glioblastoma Xenografts

TL;DR: Daily administration of topotecan inhibits HIF-1α protein expression in U251-HRE glioblastoma xenografts and causes a significant tumor growth inhibition associated with a marked decrease of angiogenesis and expression of Hif-1 target genes in tumor tissue.