In the PomX/Y/Z cell division regulatory system, PomX is a PomZ ATPase activating protein, a scaffold for PomX/Y/Z complex formation, and important for fission of the PomX/Y/Z complex during division.

Single-cell transcriptomic analyses of hypothalamic POMC neurons performed at seven developmental ages revealed marked cellular heterogeneity and divergent developmental pathways into alternative neuronal phenotypes that lack POMC.

Efference copy dysfunctions in heightened autistic traits impair the use of eye movement information for spatial representation and object localization.

Advanced microscopy techniques reveal that clusters of Pom1 kinase at the membrane represent the functional unit that shape the concentration gradients and modulate Pom1 mid-cell levels according to cell size.

A subset of hypothalamic POMC neurons that express leptin receptors control metabolic responses to changing energy availability including regulating blood glucose and leptin levels.

The coordinated differential modulation of satiety signaling POMC- and hunger signaling AgRP- neurons in the arcuate nucleus of the hypothalamus assigns an important role to noradrenalin to promote feeding.

Feeding and fasting associated alterations in proopiomelanocortin neuronal responses to insulin coordinate glucose metabolism.

Loss miRNA maturation in proopiomelanocortin (POMC) neurons causes metabolic dysregulation and favors the differentiation of Pomc progenitors into neuropeptide Y neurons, a developmental process that appears to specifically involve miR-103/107.

Gradual changes in the firing of specific hypothalamic neurons over many hours signal falling energy levels, while short-lived changes over seconds and minutes signal the availability of food.

The development of diet-dependent obesity results in the deterioration of calcium homeostasis in pro-opiomelanocortin-expressing neurons and impaired function of the same neurons.