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Endothelial focal adhesion kinase helps tumor cells enter the bloodstream.

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Howard studies motor proteins and how they shape cell behaviors.


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S phase, G2/M phase, and spindle assembly checkpoints all cooperate to restrain mitosis transiently when replication forks are progressing normally.

During platelet activation, motor protein-induced coiling of the microtubule-based marginal band leads to the cells’ characteristic spherical shape, whereas actomyosin-mediated compression of the coil results in new microtubule polymerization in a smaller ring.


Small heat shock proteins translocate to unfolded titin Ig domains under stress conditions to prevent titin aggregation and myocyte stiffening.

Pih1d3 promotes the stability and assembly of axonemal outer and inner dynein arms to allow for cytoplasmic preassembly of dynein complexes in spermatogenic cells.

Talpid3 and Cep290 promote proper ciliary vesicle formation by regulating centriolar satellite accretion and Rab8a localization.

The mechanism of NEMO recruitment into supramolecular complexes and its dependence on ubiquitination differs in response to the proinflammatory cytokines TNF and IL-1.

Endothelial cell focal adhesion kinase is a key intermediate between c-Src and the regulation of endothelial cell barrier function in the control of tumor metastasis.


A genome-wide screen identifies 17 regulatory hubs that modulate the levels of the core cadherin–catenin complex and coordinate cadherin-mediated cell–cell adhesion.

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