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Crosstalk between the serine/threonine kinase StkP and the response regulator ComE controls the stress response and intracellular survival of Streptococcus pneumoniae.
Stress-triggered signaling affecting survival or suicide of Streptococcus pneumoniae.
Compensatory evolution of pbp mutations restores the fitness cost imposed by ß-lactam resistance in Streptococcus pneumoniae.
The pneumococcal two-component system SirRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pulmonary cells.