For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
9
views
30
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      336
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      FANCC localizes with UNC5A at neurite outgrowth and promotes neuritogenesis

      brief-report

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          The Uncoordinated 5A (UNC5A) protein is part of a family of receptors that play roles in axonal pathfinding and cell migration. We previously showed that the Fanconi anemia C protein (FANCC) interacts with UNC5A and delays UNC5A-mediated apoptosis. FANCC is a predominantly cytoplasmic protein that has multiple functions including DNA damage signaling, oxygen radical metabolism, signal transduction, transcriptional regulation and apoptosis. Given the direct interaction between FANCC and UNC5A and that FANCC interferes with UNC5A-mediated apoptosis, we explored the possibility that FANCC might play a role in axonal-like growth processes.

          Results

          Here we show that FANCC and UNC5A are localized to regions of neurite outgrowth during neuronal cell differentiation. We also show that absence of FANCC is required for neurite outgrowth. In addition, FANCC seems required for UNC5A expression. Results from this study combined with our previous report suggest that FANCC plays a role in tissue development through the regulation of UNC5A-mediated functions.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: not found

          Netrins: versatile extracellular cues with diverse functions.

          Karen Lai Wing Sun, James Correia, Timothy E. Kennedy (2011)
          Netrins are secreted proteins that were first identified as guidance cues, directing cell and axon migration during neural development. Subsequent findings have demonstrated that netrins can influence the formation of multiple tissues, including the vasculature, lung, pancreas, muscle and mammary gland, by mediating cell migration, cell-cell interactions and cell-extracellular matrix adhesion. Recent evidence also implicates the ongoing expression of netrins and netrin receptors in the maintenance of cell-cell organisation in mature tissues. Here, we review the mechanisms involved in netrin signalling in vertebrate and invertebrate systems and discuss the functions of netrin signalling during the development of neural and non-neural tissues.
          Article 0 comments Cited 158 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            A ligand-gated association between cytoplasmic domains of UNC5 and DCC family receptors converts netrin-induced growth cone attraction to repulsion.

            Kyonsoo Hong, Lindsay Hinck, Makoto Nishiyama … (1999)
            Netrins are bifunctional: they attract some axons and repel others. Netrin receptors of the Deleted in Colorectal Cancer (DCC) family are implicated in attraction and those of the UNC5 family in repulsion, but genetic evidence also suggests involvement of the DCC protein UNC-40 in some cases of repulsion. To test whether these proteins form a receptor complex for repulsion, we studied the attractive responses of Xenopus spinal axons to netrin-1, which are mediated by DCC. We show that attraction is converted to repulsion by expression of UNC5 proteins in these cells, that this repulsion requires DCC function, that the UNC5 cytoplasmic domain is sufficient to effect the conversion, and that repulsion can be initiated by netrin-1 binding to either UNC5 or DCC. The isolated cytoplasmic domains of DCC and UNC5 proteins interact directly, but this interaction is repressed in the context of the full-length proteins. We provide evidence that netrin-1 triggers the formation of a receptor complex of DCC and UNC5 proteins and simultaneously derepresses the interaction between their cytoplasmic domains, thereby converting DCC-mediated attraction to UNC5/DCC-mediated repulsion.
            Article 0 comments Cited 132 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The netrin receptor UNC5B mediates guidance events controlling morphogenesis of the vascular system.

              Q. Jiang, Li Ley, Marc Lavigne … (2004)
              Blood vessels and nerves are complex, branched structures that share a high degree of anatomical similarity. Guidance of vessels and nerves has to be exquisitely regulated to ensure proper wiring of both systems. Several regulators of axon guidance have been identified and some of these are also expressed in endothelial cells; however, the extent to which their guidance functions are conserved in the vascular system is still incompletely understood. We show here that the repulsive netrin receptor UNC5B is expressed by endothelial tip cells of the vascular system. Disruption of the Unc5b gene in mice, or of Unc5b or netrin-1a in zebrafish, leads to aberrant extension of endothelial tip cell filopodia, excessive vessel branching and abnormal navigation. Netrin-1 causes endothelial filopodial retraction, but only when UNC5B is present. Thus, UNC5B functions as a repulsive netrin receptor in endothelial cells controlling morphogenesis of the vascular system.
              Article 0 comments Cited 124 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                FengFei Huang: fengfei2med@gmail.com
                Manel Ben Aissa: benaissa@uic.edu
                Georges Lévesque: Georges.Levesque@crchul.ulaval.ca
                Madeleine Carreau:
                ORCID: http://orcid.org/0000-0002-0582-6114
                1 (418) 525-4444 , Madeleine.Carreau@crchul.ulaval.ca
                Journal
                Journal ID (nlm-ta): BMC Res Notes
                Journal ID (iso-abbrev): BMC Res Notes
                Title: BMC Research Notes
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1756-0500
                Publication date (Electronic): 12 September 2018
                Publication date PMC-release: 12 September 2018
                Publication date Collection: 2018
                Volume: 11
                Electronic Location Identifier: 662
                Affiliations
                [1 ]ISNI 0000 0001 0013 6651, GRID grid.411065.7, Centre Hospitalier Universitaire de Québec-Université Laval, CHUL, ; 2705 Boul. Laurier, RC-9800, Quebec, QC G1V 4G2 Canada
                [2 ]ISNI 0000 0004 1936 8390, GRID grid.23856.3a, Department of Psychiatry and Neurosciences, , Université Laval, ; Quebec, QC Canada
                [3 ]ISNI 0000 0004 1936 8390, GRID grid.23856.3a, Department of Pediatrics, , Université Laval, ; Quebec, QC Canada
                [4 ]Present Address: Medicinal Chemistry and Pharmacognosy, College of Pharmacy, Chicago, IL USA
                Author information
                http://orcid.org/0000-0002-0582-6114
                Article
                Publisher ID: 3763
                DOI: 10.1186/s13104-018-3763-1
                PMC ID: 6136181
                PubMed ID: 30213274
                SO-VID: c0026719-d590-41df-bba1-eacea8127ef3
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 24 July 2018
                Date accepted : 4 September 2018
                Funding
                Funded by: Canadian Institutes of Health Research
                Funded by: Fondation du CHU de Québec
                Categories
                Subject: Research Note
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Medicine
                Keywords: uncoordinated-5a,neurite outgrowth,neuritogenesis,fanconi anemia,fancc
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: uncoordinated-5a, neurite outgrowth, neuritogenesis, fanconi anemia, fancc

                Comments

                Comment on this article

                scite_

                Similar content336

                See all similar

                Cited by1

                See all cited by

                Most referenced authors263

                See all reference authors