PMID: 8971808Nov 29, 1996Paper

In growth cones of rat cerebral neurons and human neuroblastoma cells, activation of protein kinase C causes a shift from filopodial to lamellipodial actin dynamics

Neuroscience Letters
H Rösner, H Fischer

Abstract

In cultures of rat cerebral neurons addition of the protein kinase C (PKC) activator 1,2-dioctanoyl-s,n-glycerol (diC8; 5 microM) induces a transient elongation of filopodia which is followed by a striking enhancement of lamellar protrusions. After 30-40 min, lamellipodia are slowly retracted, filopodia reappear and become predominant again. The reappearance of filopodia is accelerated by addition of the potent PKC-inhibitor RO-31-8220 (2 microM). A similar transient promotion of lamellar protrusive activity is obtained in SH-SY5Y neuroblastoma cells upon stimulation by acetylcholine or diC8. Immunostainings showed that the new space created by extending actin-driven lamellipodia is rapidly entered by microtubules. Preincubation with or permanent presence of RO-31-8220 totally inhibits both filopodial and lamellipodial protrusive activity. The data suggest that both filopodial and lamellipodial protrusion require active PKC, however of different levels of activation.

References

Feb 1, 1992·Current Opinion in Cell Biology·C Cypher, P C Letourneau
Oct 1, 1994·Current Opinion in Neurobiology·C H LinP Forscher
Nov 1, 1993·Neuroscience Research·K Sobue
Feb 1, 1994·Current Opinion in Neurobiology·D Bentley, T P O'Connor
Feb 9, 1996·Cell·T J Mitchison, L P Cramer
Jan 1, 1996·Annual Review of Neuroscience·C S Goodman

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Citations

Aug 22, 2001·Molecular Biology of the Cell·M SteketeeK W Tosney
Jan 1, 2008·Cell Adhesion & Migration·Tina Rüdiger, Jürgen Bolz
Aug 17, 2002·The Journal of Biological Chemistry·Arash NakhostWayne S Sossin

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