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The ability of COPI to bind polyubiquitin is a key determinant for SNARE incorporation into intracellular vesicles and for maintenance of a functional Golgi complex.

The molecular, cellular, and spatial heterogeneity of adult human spinal cord serve as an important resource to explore the mechanisms underlying spinal cord physiology and diseases.

Silencing L2 neurons that project to C6 after a T9 contusion, effectively removing spared axons, results in improved paw placement timing and order, and normalizes speed-dependent changes in swing and stance representing a significant neuroanatomical-functional paradox for spinal cord injury.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Inactivation of the COPI vesicle coat in yeast reveals that COPI recycles early but not late Golgi proteins.

Single-cell expression profiling and genetic lineage analysis show that aging impairs adipocyte differentiation from precursor cells and blocks the thermogenic activation of adipocytes during cold exposure.

COPI vesicle coat protein recognizes a ubiquitin sorting signal on an exocytic v-SNARE to mediate recycling.

Intercellular interactions between fibrocytes and CD8⁺ T lymphocytes promote inflammation through a pathophysiological positive feedback loop in bronchi of patients with chronic obstructive pulmonary disease (COPD).

A brown-to-white adipogenic transdifferentiation process in the periureter region of mouse renal adipose tissue gives rise to a population of cold-inducible adipocytes with a transcriptome distinct from subcutaneous beige adipocytes.

Diverse muscle spindle firing, critical for a range of sensorimotor behaviors, is compactly explained by first principles of force development in specialized muscle fibers within the sensors.