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In This Issue

In Focus

Cells modify force-transmitting protein for use in adherens junctions.

People & Ideas

Mogilner uses modeling to probe and explain the behavior of cells and their cytoskeleton.



In Special Collection:
JCB65: Autophagy

PINK1 phosphorylates ubiquitin, which then binds to Parkin and activates its E3 ligase activity, leading to induction of selective autophagy of damaged mitochondria.

Live-cell imaging, combined with mapping of 3D matrix displacements, identifies sites at which cells apply contractile forces to the matrix and reveals roles for physical forces in cell division.


PKA-mediated phosphorylation of a specific residue in the dynein light intermediate chain 1 releases the motor protein from lysosomes and late endosomes while activating its recruitment to adenovirus capsids.

Mitochondrial fusion is frequent in skeletal muscle, and its disruption jeopardizes excitation–contraction coupling and may contribute to the pathology of myopathies.

ProSAP1/Shank2 and syndapin I–enriched membrane nanodomains are important spatial cues and organizing platforms that shape dendritic membranes into synaptic compartments.

Localized plasma membrane expansion during axon branching mediated by Netrin-1 occurs via TRIM9-dependent regulation of SNARE-mediated vesicle fusion.

The integral membrane glycoprotein BARP associates with voltage-gated calcium channel Cavβ subunits, disrupting their association with Cavα1 subunits and suppressing overall channel activity.

Vinculin phosphorylation on residue Y822 is necessary for cell stiffening in response to tension on cadherins but not integrins.

β3 integrin residue Y747 is required for cell spreading and paxillin adapter recruitment to substrate-bound integrins in response to substrate stiffness.

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