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In Focus

A signaling pathway directs cells to degrade peroxisomes while leaving other organelles untouched.

People & Ideas

Glimcher pursues a cross-disciplinary understanding of how cell biology affects the immune system.

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In Special Collection:
JCB65: Autophagy

Defective mitochondrial quality control is shown to be a mechanism for neurodegeneration in some forms of Parkinson's disease.

A screen in oligodendrocytes establishes a Rab family member and its GAPs as regulators of exosome secretion by controlling endocytic vesicle docking with the plasma membrane.

Article

An increased number of primer–template junctions generated by PCNA, Pol-δ, and Pol-ε at stalled replication forks activates Chk1.

A biosensor for cyclin B–Cdk1 activity shows that it uses an unconventional yet simple mechanism for nuclear accumulation.

The Hsp90–Sgt1 chaperone and the ubiquitin ligase subunit Skp1 regulate the assembly and turnover of the kinetochore complex Mis12.

Disrupting LGN’s function at lateral membrane domains displaces the axis of cell division in cyst-forming MDCK cells.

A proline-rich region in the Drosophila Pat1 homologue works with the protein's C-terminal domain to recruit decapping and deadenylase complexes to target mRNAs.

The S. cerevisiae Slt2p MAPK cascade picks out peroxisomes for autophagy-mediated degradation (pexophagy) but is not involved in turnover of other cellular components.

In the absence of moesin, RhoA slips out of its normal role as a GTPase to activate the JNK MAPK pathway and spur apoptosis.

The Notch intracellular domain and β-catenin team up with RBP-J to regulate gene transcription and promote the development of arterial endothelial cells.

αE-catenin has cell–cell contact–dependent and –independent functions in regulating actin and membrane dynamics.

The I-BAR domain–containing protein, missing-in-metastasis, directs cell motility by opposing the endocytic activity of the endophilin–CD2AP–cortactin complex.

Loss of β3 integrin enhances turnover of focal adhesions and cell migration speed due to increased β1 integrin–talin interactions.

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