Randall Johnson's Group

Our laboratory uses genetic models to study the effects of hypoxia in physiological and pathological contexts, specifically dissecting the roles of different isoforms of Hypoxia Inducible Factors (HIF) as regulators of the hypoxia response in different cell types.

One of the functions of the mammalian hypoxic response in development and cancer is the generation of nascent vascular networks through angiogenesis. Through transcriptional regulation of the vascular endothelial growth factor A (VEGF-A) and other angiogenic factors, the Hypoxia-Inducible Factors can increase angiogenesis in an oxygen dependent fashion, and gives a survival and growth advantage to HIF wild type tumors. However, their role in other cell types is not always redundant. We are starting to understand that each cell type within the tumor microenvironment has specific hypoxia response strategies that independently affect tumor growth and tumor dispersion. We use genetic techniques to identify the role of hypoxia-triggered and HIF-dependent responses in different cell types, with a particular focus on cancer.

Group members

Milos GojkovicPhD student, Graduate Student
Michael GrallaPhD student
Randall JohnsonProfessor
Helene RundqvistSenior lab manager
Niclas SandbergLaboratory engineer
Emilia SöderbergLaboratory engineer
Nikola VojnovicPhD student

Selected publications

Endothelial cell HIF-1α and HIF-2α differentially regulate metastatic success.
Branco-Price C, Zhang N, Schnelle M, Evans C, Katschinski D, Liao D, et al
Cancer Cell 2012 Jan;21(1):52-65

Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression.
Doedens A, Stockmann C, Rubinstein M, Liao D, Zhang N, DeNardo D, et al
Cancer Res. 2010 Oct;70(19):7465-75

Differential activation and antagonistic function of HIF-{alpha} isoforms in macrophages are essential for NO homeostasis.
Takeda N, O'Dea E, Doedens A, Kim J, Weidemann A, Stockmann C, et al
Genes Dev. 2010 Mar;24(5):491-501

Loss of myeloid cell-derived vascular endothelial growth factor accelerates fibrosis.
Stockmann C, Kerdiles Y, Nomaksteinsky M, Weidemann A, Takeda N, Doedens A, et al
Proc. Natl. Acad. Sci. U.S.A. 2010 Mar;107(9):4329-34

Deletion of vascular endothelial growth factor in myeloid cells accelerates tumorigenesis.
Stockmann C, Doedens A, Weidemann A, Zhang N, Takeda N, Greenberg J, et al
Nature 2008 Dec;456(7223):814-8

Cell Biology