The structure of the entire Mot1 Swi2/Snf2 protein uncovers an unexpected auto-inhibited resting state activated by substrate binding, and suggests a DNA pulling mechanism of TBP displacement.
The IGF2 mRNA binding protein-2/IMP2, overexpressed in many common cancers, drives cancer cell proliferation by increasing the abundance of IGF2 and the oncogene HMGA1, which controls a network of effectors that enhance IGF2 action.
Upon genotoxic stress, the FBXL10-RNF68-RNF2 ubiquitin ligase complex mono-ubiquitylates histone H2A and mediates H2A/H2A.Z exchange to repress transcription and ensures proper high fidelity homologous recombination repair.
Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.
The anticonvulsant drug lamotrigine inhibits bacterial ribosome biogenesis and reveals an unexplored role for initiation factor 2 (IF2) in ribosome assembly.
Neonatal mouse heart regeneration relies on the presence of mononuclear diploid cardiomyocytes, which unites this process with embryonic heart growth and adult heart regeneration.
Loss of Inverted Formin-2 impairs intracellular trafficking and trophoblast invasion, resulting in maternal hypertension and intrauterine growth restriction, which represents a novel model of impaired placental invasion that encompasses critical aspects of the great obstetrical syndromes.
A structural analysis of the transcription regulator Mot1 in complex with promoter DNA and the proteins TBP and NC2 provides a first structural framework for how a Swi2/Snf2 type remodeler interacts with a histone fold protein:DNA complex.
Mutations in TIN2, a component of shelterin that keeps telomere length in check, lead to cancer-predisposition by disabling the telomere tumor suppressor pathway.
Cation-independent-mannose-6-phosphate-receptor, or insulin-like-growth-factor-2-receptor (CIM6P/IGF2R) expressed in the hippocampus controls the protein metabolism regulated by learning and required for memory consolidation, and is also a key mechanism for memory enhancement.
