Postnatal, postsynaptic loss of FMRP specifically weakens callosal synaptic inputs onto L2/3 pyramidal neurons, in requirement ofnormal sensory experience, through downregulating AMPA receptor transmission and without affecting local synaptic inputs during cortical circuit development.

Myogenin promotes centrosome attenuation and establishes the nuclear envelope as the dominant microtubule organization center via the scaffold protein AKAP6, which is required for the recruitment of centrosomal proteins.

Irreversible differentiation into somatic cells is evolutionarily optimal if changing cell phenotype is costly, a few somatic cells already improve the organism's performance, and the organism is large enough.

The identification of SMA-miR supports the pathogenic role of skeletal muscle in spinal muscular atrophy and, integrated in the SMA-score, may help to improve the phenotypic prediction for patients.

Inhibitory cerebellar feedback to the inferior olive is central to computational models of learning, but novel targets of these neurons identified here expand their potential roles.

With unique lesion-informed tractography, left hemisphere temporo-cerebellar structural connectivity has been established, supporting rapid auditory transmission and cortical functional lateralization.

Latest advances in biological timing studies substantiate an emerging concept of autonomous clocks that are normally entrained by the cell cycle and/or the circadian clock to run in synchrony, but have evolved to run independently to regulate different cellular events.

Activity-induced dendritic calcium influx in oxytocinergic magnocellular neurons can be robustly modulated by a highly diverse set of stimuli acting on distinct types of ion channels expressed along the dendritic membrane.

An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.

Funding inequalities for NIH-supported research project grant investigators and organizations have increased over the past 25 years, but have modestly decreased over the past 3 years.