Issues

The ubiquitin ligase induces senescence by promoting degradation of the glycolytic enzyme phosphoglycerate mutase.

Papa studies adaptive and maladaptive responses to ER stress.

A Bub1–Mad1 interaction targets the Mad1–Mad2 complex to unattached kinetochores to initiate the spindle checkpoint.

Contrary to earlier findings, preperoxisomal membrane structures form in yeast cells lacking the peroxin Pex3 and are competent to mature into functional peroxisomes upon Pex3 reintroduction.

Lamins impede 3D migration but also promote survival against migration-induced stresses.

Arp5 suppresses myocardin activity through both direct binding to myocardin and binding to SRF to prevent transcriptional activation of myogenic genes by the myocardin–SRF complex.

HsSAS-6 homodimers are present in the cytoplasm and assemble into ninefold symmetrical arrays at centrosomes, thus initiating procentriole formation.

As part of a regulatory loop linking cell metabolism, growth, and proliferation, CIP2A promotes mTORC1-mediated cell growth and autophagy inhibition but is itself down-regulated by autophagy.

Mdm2, a ubiquitin ligase and downstream effector of p53, attenuates the proliferative potential of primary cells via ubiquitination and degradation of the glycolytic enzyme PGAM under senescence-inducing stress.

By promoting dissociation of the desmosomal component plakoglobin from PI3K, the ubiquitin ligase Trim32 reduces PI3K–Akt–FoxO signaling in normal and atrophying muscle, potentially contributing to insulin resistance and catabolic disorders.

PKC-dependent dynamic control of Munc18-1 levels enables individual synapses to tune their output during periods of activity.

Caveolae transduce mechanical stress into plasma membrane lipid alterations that disrupt Ras organization in an isoform-specific manner and modulate downstream signal transduction.

Endosomal sorting and fission machineries act together to produce retrograde transport carriers.

Nonspecific intermolecular collision between the central pair apparatus and radial spokes underlies a mechanosensing mechanism that regulates dynein activity in Chlamydomonas flagella.

MarvelD3 recruits MEKK1 to tight junctions, which down-regulates JNK signaling and is essential for maintaining the integrity of tight junctions and restricting cell migration and proliferation.

Expression of the transcription factor Twist1 induces dissemination of normal mammary epithelial cells without changing the RNA levels of epithelial-specific genes such as E-cadherin.