Vps29 promotes retromer localization in the adult Drosophila brain, engaging Rab7 and TBC1D5, and its loss triggers age-dependent neuronal impairments in endolysosomal trafficking and synaptic transmission.
Relocation of Rab, Ras and Rho family GTPases to the surface of mitochondria enables efficient identification of their effectors, exchange factors and GAPs by proximity biotinylation.
Integrating decades of small-scale experiments with human gene expression data provides a systems-level view of the coordinated molecular processes triggered by spinal cord injury, and their relationship to recovery.
The human leukemia virus HTLV-1 causes abnormal chromatin looping in tens of thousands of infected T cell clones in each host, and abnormal host transcription both flanking the integrated provirus and at distant loci in cis.
Rhythmic transcriptome analyses of human skeletal muscle tissue and cultured primary myotubes reveal an essential role for the circadian coordination of glucose homeostasis and lipid metabolism in human skeletal muscle.
Transcriptomic and genomic analysis provides a resource of 50 primate-specific genes preferentially expressed in neural progenitors of fetal human neocortex, 15 of which are specific to humans.
Lower mitochondrial coenzyme Q was a consistent feature across multiple in vitro and in vivo models of insulin resistance and was sufficient to cause insulin resistance through increased mitochondrial oxidants.
Parkin ubiquitination of damaged mitochondria recruits the Rab GEF, RABGEF1, to regulate downstream Rab cycles and ATG9A recruitment to growing phagophores that are participating in mitophagy.
