Nodal is assumed to be the sole inducer of mesendoderm, but the related signal Vg1 is as essential as Nodal in this process.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

Gamma-band synchronization behavior in area V1 was predicted by weakly coupled oscillator principles.

The p38 MAPK pathway functions downstream of a cell-size-sensing process to coordinate cell size/growth with G1 progression in animal cells.

The subcortical visual pathway through the midbrain superior colliculus is responsible for visually evoked Pavlovian conditioning and dopamine neuron responses with predicted value in monkeys, which remained after lesioning V1.

Two-photon imaging reveals super-sparse responses to natural images in primate V1, which carry sufficient information for discrimination of the input natural images with high accuracy.

MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.

Genetic analyses demonstrate that Gdf3/Vg1 is a maternal effect gene required for robust Nodal signaling during different phases of embryogenesis including germ-layer formation, Kupffer's vesicle morphogenesis, and left-right patterning.

Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.

Heterogeneity of neural responses in mouse cortex correlates better with visual detection than mean population activity.