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Heat shock protein 90 (HSP90) is a chaperone that facilitates protein folding. In diseased cells, HSP90 and its co-chaperones form oligomers, known as epichaperomes, that confer aberrant scaffolding and holding functions onto the chaperone.
Vascular endothelial growth factor A (VEGFA) is an important regulator of angiogenesis. Increasing knowledge of its role in pathophysiology has culminated in the wide use of anti-VEGFA agents in oncology and in the treatment of neovascular eye disorders, and has opened avenues for promoting tissue vascularization in regenerative medicine.
All aspects of gene regulation involve RNA helicases, which bind or remodel RNA and RNA–protein complexes. Recent data establish a link between helicase structure, mechanism of function and biological roles, including in diseases such as cancer and neurological disorders, with implications for the design of small-molecule inhibitors.
BCL-2 proteins fulfil important functions in cell death as initiators, guardians and executioners of mitochondrial outer membrane permeabilization. Recent findings demonstrating complex interactions among BCL-2 proteins set forth a comprehensive model of BCL-2 action.
Nucleobase modifications are prevalent in eukaryotic mRNA and are broadly required for post-transcriptional gene regulation. The most studied mRNA modification is N6-methyladenosine (m6A), yet various other modifications are now being identified and studied. This Review discusses the emerging mechanisms and roles of these non-m6A modifications.
Single-cell multi-omics methods are essential for characterizing cell states and types. The past decade has ushered in improvements in spatial resolution and computational data integration and in new omics modalities. Consequently, single-cell multi-omics have advanced fundamental and translational research, including, for example, in production of cell atlases and in tumour immunology therapeutics.
Actin is most frequently associated with cell migration and shape control. However, actin has a multitude of other cellular roles, including regulating the function and dynamics of organelles. This Review discusses a plethora of actin functions in mitochondrial biology.
Structural maintenance of chromosomes (SMC) complexes, which connect regulatory DNA elements, form chromatin loops and hold together sister chromatids, are required for accurate chromosome segregation and of control transcription, replication and DNA repair. It has recently become clear that SMC complexes also control nuclear organization by counteracting clustering between similar chromatin regions.
Skeletal muscles show high metabolic flexibility and functional plasticity in their response to different exercise modalities. Recent findings have advanced our understanding of signalling, transcriptional and epigenetic mechanisms that regulate muscle adaptation to exercise and their impact on muscle physiology.
Phospholipids are asymmetrically distributed between membrane leaflets but change their location in various biological processes, which requires designated proteins — flippases and scramblases. Recent insights into the functional mechanisms of these proteins pave the way for better understanding of the roles of membrane asymmetry and the (patho)physiological consequences of its disruption.
Spindle assembly during cell division requires self-organization of microtubules into a complex, bipolar structure that directs the movement of chromosomes. Recent advances reveal the emergent properties of the spindle, most importantly its mechanical features, that facilitate robust assembly and chromosome segregation.
The spindle assembly checkpoint (SAC) ensures correct chromosome segregation during mitosis by inhibiting anaphase until all kinetochores are attached to microtubules. Recent studies highlight the dynamic properties of SAC signalling and begin to explain signal integration at mammalian kinetochores, which feature multiple attachment points.
Pools of quiescent adult stem cells support tissue turnover and regeneration in mammals. Recent studies shed new light on the roles of post-transcriptional mechanisms in controlling entry into, maintenance of and exit from the quiescent state, with important implications for regenerative medicine.
Autophagy can serve both tumour-suppressive and tumour-promoting roles, often depending on disease stage and mutational background. Recent findings have advanced our understanding of these seemingly opposing roles of autophagy in cancer cells themselves and in the tumour microenvironment.
Mechanical cues from the extracellular matrix (ECM) regulate cell fate and behaviour through cell–ECM mechanotransduction. Studies of cell–ECM mechanotransduction have largely focused on cells cultured in 2D, and only recently have we begun to unravel how these processes occur in 3D — a context native to many cells in vivo.
CRISPR-based genetic screens are providing new insights into the consequences of deficiencies in DNA damage response and repair pathways. These include insights into the regulation of homologous recombination and of replication stress and their crosstalk with other repair pathways, into novel cancer therapies and into the basis of cancer-drug resistance.
Extracellular vesicles (EVs) have emerged as important players in intercellular communication, carrying proteins, lipids, nucleic acids and various signalling molecules between cells. Unravelling how these different cargoes are sorted into EVs in a regulated and context-specific manner is essential to understanding the specificity of EV-mediated signalling.
Ribosome biogenesis, including ribosomal RNA (rRNA) production, occurs in the nucleolus. Recent studies have revealed how the integrity and copy number of rRNA genes is maintained through a unique recombination system, how rRNA transcription is regulated and how phase separation orchestrates nucleolus function.
Metabolites are generally viewed as intermediates or products of metabolism. However, many metabolites are also signalling molecules that regulate metabolic reactions and other processes in development, homeostasis and disease. As such, metabolites can confer adaptive responses to environmental changes.
The inability of the mammalian central nervous system to functionally regenerate after injury is largely attributable to the limited capacity of injured neurons to regrow axons. In the spinal cord, recent work on the mechanisms restricting axon regrowth suggests new therapeutic avenues to promote functional recovery after damage.
