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Mathematical modeling shows how RAF inhibitors can actually activate RAF kinases by stabilizing RAF proteins in the conformation capable of dimerization.

The sensory regulatory system of the cholera causative involves the detection of bile acids by direct interaction with the inner membrane protein complex formed by ToxR and ToxS, thereby inducing concentration-dependent structural changes.

Acetate concentration, which is significantly increased in association with energy stresses such as those that occur with diabetes or starvation, is emerging as a novel 'ketone body' with potential as a parameter for evaluating the progression of energy stress.

The enterococcal adhesin PrgB consists of four immunoglobulin-like domains that support the proper function of its polymer adhesin domain.

Why do some inhibitors select the on-state in ERK2, a kinase that is involved in many signaling pathways in cells, whereas others bind to more than one conformation?

Carefully controlling the level of protein synthesis reduction and mode of translation inhibitor action reveal different and sometimes opposing phenotypic effects following proteostasis stress, wherein protection via initiation inhibition specifically depends on heat shock factor 1.

A subtle mutation in the ATP-binding site of inositol hexakisphosphate kinases increases their conformational flexibility and thereby makes them susceptible to isozyme-selective, allosteric inhibition.

Inducing the formation of mitochondrial respiratory chain supercomplexes in Drosophila melanogaster, where they are normally absent, does not have any noticeable impact in the function of the respiratory chain.

Live human pancreatic α-cells can be purified effectively using zinc-based reaction probe diacetylated Zinpyr1 and cultured as pseudoislets without losing their viability and function.

Deletion of optic atrophy 1 in brown adipose tissue induces secretion of growth differentiation factor 15 as a batokine to attenuate diet-induced obesity and improve glucose clearance, hepatic steatosis, and thermoregulation in mice by increasing energy expenditure.