Colored surfaces induce strong gamma-synchronization yet sparse firing in V1 when receptive field inputs are predicted from the surrounding spatial context.
In G1 cells, Scc2 loads and maintains cohesin on chromosomes by counteracting a Wapl-independent releasing activity, which is neutralized in S phase by CDK1.
Cells accumulate damaged proteins during aging and, by compromising the function of chaperones in folding newly synthesized G1 cyclins, proteostasis breakdown inhibits cell-cycle entry and drives yeast cells into senescence.
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.
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.
A peptide derived from BK and JC polyomavirus protein VP2/3 inhibits viral infection by targeting a binding site in the pore of polyomavirus VP1 pentamers, enabling future VP1-targeted therapeutic strategies.
Two phosphorylation sites on 53BP1 are found to mediate interaction with TOPBP1-RAD9 and shown to be essential for assembling the G1 DNA damage checkpoint response apparatus.
