ArticleExperimental cell research2010
Induction of filopodia-like protrusions by transmembrane agrin: role of agrin glycosaminoglycan chains and Rho-family GTPases.
Article in Experimental cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Review
- Overexpression of Isoforms of Nitric Oxide Synthase 1 Adaptor Protein, Encoded by a Risk Gene for Schizophrenia, Alters Actin Dynamics and Synaptic Function.Frontiers in cellular neuroscience · 2016Article
- An oncogenic role of Agrin in regulating focal adhesion integrity in hepatocellular carcinoma.Nature communications · 2015Article
- ECM receptors in neuronal structure, synaptic plasticity, and behavior.Progress in brain research · 2014Review
- DPP6 regulation of dendritic morphogenesis impacts hippocampal synaptic development.Nature communications · 2013Article
- The role of agrin in synaptic development, plasticity and signaling in the central nervous system.Neurochemistry international · 2012Review
- mDia1 and WAVE2 proteins interact directly with IRSp53 in filopodia and are involved in filopodium formation.The Journal of biological chemistry · 2012Article
- A valid mouse model of AGRIN-associated congenital myasthenic syndrome.Human molecular genetics · 2011Article
- Casting a net on dendritic spines: the extracellular matrix and its receptors.Developmental neurobiology · 2011Review
- Emerging roles for MAP kinases in agrin signaling.Communicative & integrative biology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Filopodia sense the extracellular environment and direct movement in many cell types, including neurons. Recent reports suggest that the transmembrane form of the widely expressed proteoglycan agrin (TM-agrin) regulates formation and stability of neuronal filopodia. In order to elucidate the mechanism by which TM-agrin regulates filopodia, we investigated the role of agrin's glycosaminoglycan (GAG) chains in the induction of filopodia formation by TM-agrin over-expression in hippocampal neurons, and in the induction of filopodia-like processes in COS7 cells. Deletion of the GAG chains of TM-agrin sharply reduced formation of filopodia-like branched retraction fibers (BRFs) in COS7 cells, with deletion of the heparan sulfate GAG chains being most effective, and eliminated filopodia induction in hippocampal neurons. GAG chain deletion also reduced the activation of Cdc42 and Rac1 resulting from TM-agrin over-expression. Moreover, dominant-negative Cdc42 and Rac1 inhibited BRF formation. Lastly, over-expression of TM-agrin increased the adhesiveness of COS7 cells and this increase was reduced by deletion of the GAG chains. Our results suggest that TM-agrin regulates actin-based protrusions in large part through interaction of its GAG chains with extracellular or transmembrane proteins, leading to the activation of Cdc42 and Rac1.
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Registered trials
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