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Selective degradation of mature miRNAs shapes temporal miRNA expression patterns and is important for proper regulation of target genes to support normal development of Drosophila embryos.

Genetic analysis combined with whole genome sequencing elucidates mechanisms and pathways that form and prevent a specific class of genome rearrangements, foldback inversions, seen in many human cancers.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.

p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.

Substitutions in general translation initiation factor eIF1A found as recurring somatic mutations in uveal melanoma destabilize the closed conformation of the preinitiation complex at the start codon and increase discrimination against suboptimal initiation codons genome-wide.

Analysis of genome integrity in primary murine B-cells reveals how depleting 26S proteasome activity enhanced cell survival following treatment with topoisomerase poisons.

Complex chromosomal rearrangements similar to those described in cancer and developmental syndromes occur in plants during postzygotic genome elimination, a centromeric-derived incompatibility.

Gene expression timing during Drosophila development is specified by multiple classes of RNA polymerase II core promoters, and the embryonic transcriptome includes thousands of evolutionarily conserved long noncoding RNAs.

The MCM-binding protein (MCMBP) promotes the hexamer assembly of the replicative MCM2–7 helicase by interacting with the nascent MCM3 subunit, playing a key role in achieving high expression levels of the functional MCM2–7 helicase for maintaining genome integrity.