7 research outputs found
Italian and American progress toward Inclusive Education: common concerns and future directions
Abstract Over the past two years, six sets of Italian scholars have responded to questions posed b
Stance time variability during stair stepping before and after total knee arthroplasty: A pilot study
Wetland Loss in Louisiana
This loss is the result of a variety of complex interactions among a number of physical, chemical, biological, and cultural processes. Important geologic phenomena include sea-level change, subsidence, compaction, and change in location of deltaic depocenters. Of the many catastrophic events that cause erosion, the hurricane with its high energy, is the most important in Louisiana. Biological factors include rates of marsh growth and the degradation caused by marsh fauna. -from Author
Myristoylated, Alanine-rich C-Kinase Substrate Phosphorylation Regulates Growth Cone Adhesion and Pathfinding
Repellents evoke growth cone turning by eliciting asymmetric, localized loss of actin cytoskeleton together with changes in substratum attachment. We have demonstrated that semaphorin-3A (Sema3A)-induced growth cone detachment and collapse require eicosanoid-mediated activation of protein kinase Cε (PKCε) and that the major PKCε target is the myristoylated, alanine-rich C-kinase substrate (MARCKS). Here, we show that PKC activation is necessary for growth cone turning and that MARCKS, while at the membrane, colocalizes with α(3)-integrin in a peripheral adhesive zone of the growth cone. Phosphorylation of MARCKS causes its translocation from the membrane to the cytosol. Silencing MARCKS expression dramatically reduces growth cone spread, whereas overexpression of wild-type MARCKS inhibits growth cone collapse triggered by PKC activation. Expression of phosphorylation-deficient, mutant MARCKS greatly expands growth cone adhesion, and this is characterized by extensive colocalization of MARCKS and α(3)-integrin, resistance to eicosanoid-triggered detachment and collapse, and reversal of Sema3A-induced repulsion into attraction. We conclude that MARCKS is involved in regulating growth cone adhesion as follows: its nonphosphorylated form stabilizes integrin-mediated adhesions, and its phosphorylation-triggered release from adhesions causes localized growth cone detachment critical for turning and collapse