scispace - formally typeset
A

Adam J. Krieg

Researcher at Oregon Health & Science University

Publications -  34
Citations -  2010

Adam J. Krieg is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Cancer & Signal transduction. The author has an hindex of 23, co-authored 31 publications receiving 1709 citations. Previous affiliations of Adam J. Krieg include University of Illinois at Urbana–Champaign & Stanford University.

Papers
More filters
Journal ArticleDOI

Regulation of the Histone Demethylase JMJD1A by Hypoxia-Inducible Factor 1α Enhances Hypoxic Gene Expression and Tumor Growth

TL;DR: It is demonstrated that loss of JMJD1A is sufficient to reduce tumor growth in vivo, demonstrating that histone demethylation plays a significant role in modulating growth within the tumor microenvironment.
Journal ArticleDOI

Direct regulation of GAS6/AXL signaling by HIF promotes renal metastasis through SRC and MET.

TL;DR: It is demonstrated that inactivation of growth arrest-specific 6 (GAS6)/AXL signaling using a soluble AXL decoy receptor reversed the invasive and metastatic phenotype of clear cell renal cell carcinoma (ccRCC) cells.
Journal ArticleDOI

AXL is an Essential Factor and Therapeutic Target for Metastatic Ovarian Cancer

TL;DR: In this article, the soluble human AXL receptors that imposed a specific blockade of the GAS6/AXL pathway had a profound inhibitory effect on progression of established metastatic ovarian cancer without normal tissue toxicity.
Journal ArticleDOI

Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes

TL;DR: It is shown that acute deletion of hepatic Phd3, also known as Egln3, improves insulin sensitivity and ameliorates diabetes by specifically stabilizing Hif-2α, which then increases Irs2 transcription and insulin-stimulated Akt activation.
Journal ArticleDOI

The metastasis-associated gene Prl-3 is a p53 target involved in cell-cycle regulation.

TL;DR: This work identifies Prl-3 (phosphatase of regenerating liver-3) as a p53-inducible gene and demonstrates that basal level PrL-3 expression is pivotal for normal cell-cycle progression, and highlights key dose-dependent functions in both positive and negative regulation of cell- cycle progression.