A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca²⁺-dependent Cl^- current in human RPE.

Cryo-EM structures of the gating cycle of bestrophin reveal the molecular underpinnings of activation and inactivation gating in this calcium-activated chloride channel and reveal a surprisingly wide pore.

The inhibition of colorectal cancer (CRC) proliferation, migration, and invasion is attributed to BEST4, which exhibits epistasis over Hes4 in the downregulation of Twist1 and consequent suppression of epithelial-to-mesenchymal transition in CRC.

BEST1 autosomal dominant loss-of-function mutations surprisingly behave in a dominant-negative manner, whereas gain-of-function mutations exhibit a strong dominant effect that necessitates CRISPR/Cas9-mediated suppression of the endogenous mutant allele in gene therapy.

Structural and functional analysis of a recently discovered non-canonical potassium channel family reveals a unique selectivity filter that is exposed to permeating ions only in the conductive state.

The reduction of bicarbonate secretion into the airways reproduces cystic fibrosis-like features, independently of chloride secretion.

GABAergic neurons in the nervous system of C. elegans have been comprehensively mapped allowing analysis of regulatory factors that program GABAergic neuron identity.

Pigmentation that confers protective function of RPE is not underlaid by a specific gene expression profile, reviled by microscopic imaging together with single-cell RNA sequencing.

Adapting bacteria to use an introduced metabolic pathway recapitulates natural mutations and offers a novel bioremediation strategy.

Skin cells from a patient with retinitis pigmentosa have been used to generate induced pluripotent stem cells, which could potentially form the basis of new treatments for this disease.