<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(6)</volume><submitter>Li J</submitter><pubmed_abstract>SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UN</pubmed_abstract><journal>PloS one</journal><pagination>e65658</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3680500</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The SAX-3 receptor stimulates axon outgrowth and the signal sequence and transmembrane domain are critical for SAX-3 membrane localization in the PDE neuron of C. elegans.</pubmed_title><pmcid>PMC3680500</pmcid><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Pu P</pubmed_authors><pubmed_authors>Le W</pubmed_authors></additional><is_claimable>false</is_claimable><name>The SAX-3 receptor stimulates axon outgrowth and the signal sequence and transmembrane domain are critical for SAX-3 membrane localization in the PDE neuron of C. elegans.</name><description>SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UN</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2025-04-26T20:27:36.839Z</modification><creation>2019-03-26T23:14:45Z</creation></dates><accession>S-EPMC3680500</accession><cross_references><pubmed>23776520</pubmed><doi>10.1371/journal.pone.0065658</doi></cross_references></HashMap>