Skip to Main Content


Skip Nav Destination


In This Issue

In Focus

Kinetochore protein might not recruit key parts of spindle assembly checkpoint and instead might help silence the checkpoint.

People & Ideas

Grinstein studies how phagocytes clean up pathogens and the mess left behind by cell death.



Autophagosome biogenesis and maturation in primary neurons is a constitutive process that is spatially and temporally regulated along the axon.


Integration of EM, protein–protein interaction, and phenotypic data reveals novel insights into the structure and function of the nuclear pore complex’s ∼600-kD heptameric Nup84 complex.

Importin-β binds RANBP2 and RANGAP1 and antagonizes CRM1 activity during RANGAP1 recruitment to kinetochores.

Structure–function studies reveal that the tetratricopeptide repeats of Bub1 and BubR1 are important for interaction with Kln1, but a distinct Bub3-binding domain is critical for kinetochore recruitment of Bub1.

A microtubule-binding site in the extreme N terminus of KNL-1 is dispensable for load-bearing attachments but participates in checkpoint silencing at the kinetochore.

Arf6 positively regulates autophagosome membrane biogenesis by inducing PIP2 generation and PLD activation, which together may influence endocytic uptake of plasma membrane into autophagosome precursors.

Alternative NF-κB signaling modulates the activity of PGC-1β to promote oxidative metabolism in skeletal muscle.

Differences in expression level of the effector caspases Drice and Dcp-1 and in their intrinsic abilities to induce apoptosis and to control the rate of cell death underlie the differential sensitivities of cells to apoptosis.

Neuropeptide signaling, which is known to affect synaptic function in neural communication, also promotes neuromuscular junction growth in Drosophila.


Close Modal

or Create an Account

Close Modal
Close Modal