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HDL particles transport cholesterol and contain apolipoprotein A-I as their major protein. The solution structure of discoidal HDL particles reconstituted with a shortened apoA-I is now solved via a combination of NMR and EPR analyses.
The crystal structure of MurJ, a bacterial lipid II flippase involved in peptidoglycan biosynthesis and a member of the MOP transporter superfamily, reveals an inward-facing conformation and points to an alternating-access mechanism.
Genome-wide analyses of S. cerevisiae replisome mobility reveal overlapping roles of Pif1 and Rrm3 helicases in alleviating replication-fork arrest at tRNA genes.
Crystal structures of human APOBEC3A and a chimera of APOBEC3B and APOBEC3A bound to ssDNA reveal an unanticipated ‘U-shaped’ binding mode and provide insight into target selectivity.
The structure of GlyRα3 in complex with a selective potentiator that decreases neuropathic pain in an animal model identifies a novel allosteric regulatory mechanism.
The cryo-EM structure of human polycystin-2 (PC2) in a closed conformation reveals a domain located above the pore filter, forming an upper vestibule and making contacts with the pore and voltage-sensor-like domains.
Cryo-EM analysis captures three states of the human Rad51 recombinase and visualizes structures of presynaptic and postsynaptic filaments as well as a synaptic complex in the process of DNA-strand exchange.
The binding sites for the anticoagulant drug warfarin and for vitamin K on the human VKOR are determined through biochemistry and computational approaches. The results indicate a competitive mechanism of inhibition of VKOR by warfarin.
Although oxidative stress has long been considered to be a major factor contributing to telomere shortening, recent work has established that oxidative stress and DNA damage are linked to telomere lengthening. Now, Opresko and colleagues resolve this apparent discrepancy by showing that differential modulation of telomerase activity depends on the origin of a common oxidative guanine lesion.
Daily rhythms are a constant part of life. This special Focus issue explores the molecular mechanisms that underlie the generation of circadian dynamics.
This Perspective focuses on five distinct regulatory elements that have been recognized as being critical for generating and modulating oscillatory dynamics in time and space, in both natural and synthetic biological networks.
In this Review, the authors consider the functions of key clock transcription factors and the epigenetic regulatory mechanisms that direct circadian gene expression in mammalian cells.
Clock proteins are controlled by multiple post-translational modifications during the circadian cycle. In this Review, the authors examine how post-translational modifications influence the stability, interactions and activity of mammalian clock proteins and how they contribute to proper clock function or are altered in circadian disorders.
This review explores the molecular basis of metabolic and gene-expression oscillations in the yeast Saccharomyces cerevisiae and describes how they relate to other biological time-keeping mechanisms, such as circadian rhythms.
This Review examines the molecular mechanisms underlying the plant circadian clock, highlighting the functions of transcriptional circuits and post-translational regulation in timing and describing how clock components integrate and respond to environmental signals.
A newly developed assay in yeast reveals that large-scale expansions of trinucleotide repeats can occur in a single step, rather than through several small-scale events.
Mass spectrometry and biochemical analyses reveal that the major form of VKOR found in cells features a disulfide bond between Cys51 and Cys132, and this intermediate is the target of the anticoagulant drug warfarin.
New data reveal that telomere length is maintained in human pluripotent stem cells through the opposing activities of telomerase-meditated elongation and telomere trimming mechanisms promoted by HR factors.
The enzyme FICD was previously known to AMPylate the ER-resident chaperone BiP, inactivating the chaperone. Mammalian FICD is now shown to catalyze the removal of the AMP group from BiP.