G. R. Hammond

The paper investigates PM PI4P turnover by targeting SAC1 to mitochondria, finding that ORP2 significantly affects PM PI4P levels independently of contact sites.

This paper investigates TMEM16A missense mutations in cancer, finding they promote tumor growth through altered signaling, independent of chloride flux.

The authors retract their paper due to an incorrect conclusion about ORP5's role in PI4P depletion, finding SAC1 targeting alone suffices.

The paper identifies PIP4K as a sensor and negative regulator of PI(4,5)P2 synthesis, revealing a homeostatic mechanism that tunes membrane functions.

The paper measures PI(4,5)P2 diffusion in the plasma membrane and finds that it diffuses rapidly even in regions with high effector protein density, suggesting free diffusion rather than spatial segregation.

The paper shows hypoxia causes reversible depletion of PM PI4P and PIP2, disrupting electrostatic targeting of polybasic proteins, and identifies PI4KIII and its regulators as essential for maintaining their homeostasis.

The paper shows that Salmonella and Shigella effectors generate PtdIns(3,4)P2 independently of phosphoinositide 3-kinases using a phosphotransferase mechanism.

The study maps the subcellular distribution of phosphatidylinositol (PI) and finds it is largely absent from the plasma membrane, where it is mainly present as PI4P and PI(4,5)P2.

The paper develops a high-avidity biosensor for PI(3,4)P2, revealing it is mainly produced by class I PI3K and hydrolyzed by PTEN.