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LeishBASEedit enables gene editing in Leishmania without requiring DNA double-strand breaks, homologous recombination, or donor DNA, thereby facilitating loss-of-function screens via delivery of plasmid libraries and regardless of limitations due to gene copy number variations and/or lack of RNAi components.

The adaptor protein Grb2 is able to enhance the activity of the cytoplasmic tyrosine kinase Btk through a novel mechanism, revealing a new role for Grb2 in B-cell signaling.

A high-throughput method to profile tyrosine kinases and phosphotyrosine recognition domains reveals new rules for sequence specificity and maps the effects of mutations on the recognition of tyrosine phosphorylation sites.

Combined patch-clamp fluorometry with ANAP, a fluorescent non-canonical amino acid, uncovers transitions in the activation pathway of human H_V1 that are modulated by voltage and the pH gradient.

Comparision of current and fluorescent kinetics from P2X7 receptor mutants labeled with the fluorescent amino acid ANAP suggests that the characteristic P2X7 current facilitation involves changes in channel gating rather than interactions or conformational changes of its intracellular ballast domain.

A sophisticated classical mutagenesis assay with next-generation sequencing technology presents a benefit to future research on mutagenesis, DNA repair, and cancer.

The entry glycoproteins of hepatitis C virus, E1E2, possess a novel regulatory mechanism in which protein disorder is harnessed to control their activity and their ability to evade antibodies.

DExCon, LUXon, and DExogron approaches simultaneously block endogenous gene expression and permit tuning of re-expression levels in time and space; proof-of-principle reveals unforeseen differences in protein kinetics, cargo handling, and cell migration regulation between closely related Rab11 family members.

Bacterial warfare protein colicin E1 opens its hinge to plug antibiotic efflux pump TolC and potentiate antibiotics.

A deep mutational scan of the ADAR2 deaminase domain creates a map for designing tailored ADAR2 variants, and splitting the deaminase between residues 468 and 469 enables highly transcript-specific RNA editing.