Skip to Main Content

Advertisement

Skip Nav Destination

Issues

In This Issue

In Focus

Study reveals that mutations in DNA-dependent protein kinase block multiple DNA repair pathways.

People & Ideas

Amon studies how cells segregate their chromosomes and what happens when they get it wrong.

Review

Report

The DNA damage checkpoint protein MDC1 also interacts with TopBP1 to promote DNA replication checkpoint control.

Impaired autophagy stabilizes p62 and promotes tumorigenesis through activation of the Nrf2 transcription factor.

Chromosome passenger complexes and bipolar kinesins act together to coordinate spindle elongation, spindle breakdown, and mitotic exit.

Article

Phosphorylation of DNA-PKcs is essential for activation of DNA damage repair and for the maintenance of tissue stem cell populations.

Centrin-null cells undergo normal division but are highly sensitive to UV irradiation as a result of impaired DNA repair.

In the absence of Tara, Trio binds to E-cadherin and increases activation of the E-cadherin transcriptional repressor Tbx3.

Electron tomography of continuous ER domains during budding shows that reticulons and Yop1 stabilize rather than generate membrane curvature in this organelle.

PKA RIα subunit is localized to MVBs by the A-kinase–anchoring protein AKAP11 when disassociated from the PKA catalytic subunit.

The cytoplasmic concentration of G-actin is a critical parameter for determining the extent of stimulus-induced G-actin assembly and cell extension.

Myosin IIA and IIB synergistically generate front–back polarity through their effects on actomyosin bundling formation and stability, and adhesion maturation, which are mediated by localized Rac GEF depletion.

Cdk2 is not essential for oligodendrocyte maturation and myelination during development, but in response to demyelination, it is required for oligodendrocyte precursor cell proliferation (OPC), and its loss accelerates OPC differentiation and remyelination.

The microRNA miR-22 targets CDK6, SIRT1, and Sp1—genes involved in regulation of the senescence program—to suppress cell growth and proliferation.

Close Modal

or Create an Account

Close Modal
Close Modal