Using genetics, it is possible to uncouple higher adiposity from its adverse metabolic effects and show that some obesity-associated conditions may benefit from treating the metabolic effects alone, whilst others may benefit more from weight loss.

Association of curvature generating proteins to the Golgi membranes by sphingomyelin metabolism essentially controls the flatness of a Golgi cisterna that is necessary for efficient sorting and export.

Sequences at mitochondrial genome recombination sites are dually used as mRNAs and as rRNAs in actively translating mitoribosomes of T. gondii.

Computational evolutionary model to predict the efficacy of broadly neutralizing antibodies (bNAbs) in suppressing HIV and to design optimal combination therapy with bNAbs.

Chemotherapeutics altering DNA topology evoke RNA polymerase I inhibition, rDNA damage and consequent formation of PNAs that segregate persistent rDNA lesions from the active nucleolus, with implications for rDNA maintenance and design of new cancer treatment strategies targeting rDNA repair.

In astrocytes, there exists an intrinsic spatial threshold of subcellular calcium levels that triggers an astrocyte calcium surge throughout the cell, demonstrating cellular astrocyte calcium integration of time and space.

Structural biology studies reveal the importance of protein dynamics on understanding molecular mechanisms underlying allosteric modulation of G protein-coupled receptors (GPCR) that offer insights into future GPCR research and drug discovery.

Novel components in the pathway from malignant hyperthermia to diabetes include promotion of a kinase that impedes glycogen synthesis, increased lysis of junctophilin1 and gene regulatory actions by a junctophilin fragment, surprisingly predicted to oppose the effects of elevated calcium.

Combining particle tracking in living cells with statistical analysis demonstrates how the oligomeric organization of cell surface receptor influences their function, a necessary step in the development of drugs targeting specific receptor conformation.

Two genetic mouse models for HCN1-linked developmental epileptic encephalopathy display distinct biophysical changes in HCN1 ion channel properties but similar worsening of seizures in response to antiepileptic drugs, thereby recapitulating key features of the human disease.