Luke W. Thomas

TL;DR: The relationship between HIF-regulated signalling pathways and the mitochondria is explored, including the regulation of mitochondrial metabolism, biogenesis and distribution, in both physiological and pathophysiological contexts.

TL;DR: Reconstitution of wild-type VHL protein in pVHL-defective renal carcinoma cells not only suppresses HIF activation and tumor growth, but also enhances mitochondrial respiratory chain function via mechanisms that are not fully elucidated.

TL;DR: The study demonstrates that the intracellular distribution of the mitochondrial network is an important feature of the cellular response to hypoxia, contributing to hypoxic signaling via HIF activation and regulated by way of the cross talk between CHCHD4 and HIF-1α.

TL;DR: It is found that under basal conditions, endogenous CHCHD4 redox state in cultured cells and mouse tissues was predominantly oxidized, however, degrees of oxidation in different tissues varied from 70% to 90% oxidized.

TL;DR: CHCHD4 drives tumour cell growth and activates mTORC1 signalling through its control of respiratory chain mediated metabolism and complex I biology, and also regulates EMT-related phenotypes of tumour cells.