ArticleMolecular biology of the cell1998
B-50/GAP-43-induced formation of filopodia depends on Rho-GTPase.
Article in Molecular biology of the cell, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 33 citations in OpenAlex.
- A role for α-Synuclein in axon growth and its implications in corticostriatal glutamatergic plasticity in Parkinson's disease.Molecular neurodegeneration · 2020Article
- Lentiviral-Mediated Netrin-1 Overexpression Improves Motor and Sensory Functions in SCT Rats Associated with SYP and GAP-43 Expressions.Molecular neurobiology · 2017Article
- hnRNP-Q1 represses nascent axon growth in cortical neurons by inhibiting Gap-43 mRNA translation.Molecular biology of the cell · 2016Article
- Smn depletion alters profilin II expression and leads to upregulation of the RhoA/ROCK pathway and defects in neuronal integrity.Journal of molecular neuroscience : MN · 2007Article
- Molecular mechanisms, biological actions, and neuropharmacology of the growth-associated protein GAP-43.Current neuropharmacology · 2006Article
- Three functionally distinct adhesions in filopodia: shaft adhesions control lamellar extension.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Biochemical, electron microscopic and immunohistological observations of cationic detergent-extracted cells: detection and improved preservation of microextensions and ultramicroextensions.BMC cell biology · 2001Article
- Local accumulations of B-50/GAP-43 evoke excessive bleb formation in PC12 cells.Molecular neurobiology · 1999Article
- Myelin and collapsin-1 induce motor neuron growth cone collapse through different pathways: inhibition of collapse by opposing mutants of rac1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Paralemmin, a prenyl-palmitoyl-anchored phosphoprotein abundant in neurons and implicated in plasma membrane dynamics and cell process formation.The Journal of cell biology · 1998Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study we show that expression of the neural PKC-substrate B-50 (growth-associated protein [GAP-43]) in Rat-1 fibroblasts induced the formation of filopodial extensions during spreading. This morphological change was accompanied by an enhanced formation of peripheral actin filaments and by accumulation of vinculin immunoreactivity in filopodial focal adhesions, colocalizing with B-50. In time lapse experiments, the B-50-induced filopodial extensions were shown to stay in close contact with the substratum and appeared remarkably stable, resulting in a delayed lamellar spreading of the fibroblasts. The morphogenetic effects of the B-50 protein were entirely dependent on the integrity of the two N-terminal cysteines involved in membrane association (C3C4), but were not significantly affected by mutations of the PKC-phosphorylation site (S41) or deletion of the C terminus (177-226). Cotransfection of B-50 with dominant negative Cdc42 or Rac did not prevent B-50-induced formation of filopodial cells, whereas this process could be completely blocked by cotransfection with dominant negative Rho or Clostridium botulinum C3-transferase. Conversely, constitutively active Rho induced a similar filopodial phenotype as B-50. We therefore propose that the induction of surface extensions by B-50 in spreading Rat-1 fibroblasts depends on Rho-guanosine triphosphatase function.
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