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People & Ideas
Central nervous system injury results in the release of molecules that inhibit neuronal regeneration, but retinoic acid counteracts this effect by inhibiting Lingo-1.
Meiotic nuclear divisions in budding yeast require PP2ACdc55-mediated antagonism of Net1 phosphorylation by Cdk
PP2ACdc55 opposes the phosphorylation of Net1 by Cdk to control meiotic nuclear divisions in budding yeast.
Cohesin, condensin, and the intramolecular centromere loop together generate the mitotic chromatin spring
During mitosis, spindle microtubule force is balanced by the combined activities of the cohesin and condensin SMC complexes and intramolecular pericentric chromatin loops.
Cdc42 regulates cardiac function in mice and flies downstream of a conserved Tinman/Nkx2-5–miR-1 signaling network.
miR669a and miR669q inhibit postnatal cardiac progenitor differentiation by directly targeting the 3′UTR of MyoD.
The PP2A regulatory subunit Cdc55 fine tunes the sequence and timing of both meiotic chromosome segregation events by limiting the activity of other phosphatases.
Before chromosome expulsion into polar bodies during female meiosis, the APC inhibits CDK-1 to allow dynein-driven spindle rotation.
The p25 subunit of the dynactin complex is required for the interaction between cytoplasmic dynein and early endosomes but is not required for dynein-mediated nuclear distribution.
Pannexin 3 functions as an ER Ca2+ channel, hemichannel, and gap junction to promote osteoblast differentiation
Pannexin 3 functions as an essential protein for Ca2+ and ATP transport and cell–cell communication during osteoblast differentiation
Inhibition of p110α or of the downstream PI3K signaling pathway components PDK1 and Akt, as well as phosphoinositide sequestration, blocks invadopodia formation in breast cancer cells.
Pak1 regulates focal adhesion strength, myosin IIA distribution, and actin dynamics to optimize cell migration
p21-activated kinases are essential for spatial and temporal coordination of cytoskeletal dynamics with cellular adhesion during cell migration.
SPARC prevents endoglin association with αV integrin, which blocks the activation of TGF-β signaling and promotes pericyte migration to nascent blood vessels.