Inhibiyiton of the lysosomal chloride-proton antiporter ClC-7 by the signaling lipid PI(3,5)P2 is important for lysosomal pH maintenance and is disrupted by a disease-causing gain-of-function mutation.

The sharp expression pattern driven by a classic, simple animal enhancer is determined by multiple molecular mechanisms, not only cooperative binding of the activating transcription factor as was previously thought.

Synergistic interactions with PI(4,5)P2 and activated Rho1, which are enriched at the apical membrane of tubular organs, facilitate tight apical targeting of the formin Diaphanous.

Proper gut health depends on the balance between two naturally occurring variants of a transcription factor in the colon.

When challenged by energetic stresses triggered by hypoxia and ATP inhibition, plasma membrane PI4P and PIP2 in cells undergo dramatic turnovers that have profound impact on many cellular processes including electrostatic PM targeting of numerous polybasic proteins.

The hunchback transcription features are compatible with an equilibrium model with a short decay length Bicoid activity gradient as the sole source of positional information, while Zelda and Hunchback speed-up the process by different means.

Genetic lesions that compromise the ribosome P-stalk implicate direct signalling from the ribosome to the translation initiation factor eIF2 kinase GCN2 in the cellular response to amino acid starvation.

A new biochemical method tests whether or not the pre-existing RNA structural correlations couple small molecule binding to gene expression in a paradigmatic riboswitch.

voyAGEr is an online platform that facilitates the exploration of age-related gene expression dynamics in human tissues, allowing users to analyse tissue- and sex-specific changes alongside donor medical histories.

Design and characterization of allosteric mutations that recapitulate TRPML1 gating and structural insights into PI(4,5)P₂ and sphingomyelin inhibition of TRPML1.