Relevant bibliographies by topics / Axon guidance

Academic literature on the topic 'Axon guidance'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Axon guidance"

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Kim, Sung Wook, and Kyong-Tai Kim. "Expression of Genes Involved in Axon Guidance: How Much Have We Learned?" International Journal of Molecular Sciences 21, no. 10 (May 18, 2020): 3566. http://dx.doi.org/10.3390/ijms21103566.

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Neuronal axons are guided to their target during the development of the brain. Axon guidance allows the formation of intricate neural circuits that control the function of the brain, and thus the behavior. As the axons travel in the brain to find their target, they encounter various axon guidance cues, which interact with the receptors on the tip of the growth cone to permit growth along different signaling pathways. Although many scientists have performed numerous studies on axon guidance signaling pathways, we still have an incomplete understanding of the axon guidance system. Lately, studies on axon guidance have shifted from studying the signal transduction pathways to studying other molecular features of axon guidance, such as the gene expression. These new studies present evidence for different molecular features that broaden our understanding of axon guidance. Hence, in this review we will introduce recent studies that illustrate different molecular features of axon guidance. In particular, we will review literature that demonstrates how axon guidance cues and receptors regulate local translation of axonal genes and how the expression of guidance cues and receptors are regulated both transcriptionally and post-transcriptionally. Moreover, we will highlight the pathological relevance of axon guidance molecules to specific diseases.
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Vactor, David Van. "Axon guidance." Current Biology 9, no. 21 (November 1999): R797—R799. http://dx.doi.org/10.1016/s0960-9822(99)80492-8.

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Zallen, J. A., S. A. Kirch, and C. I. Bargmann. "Genes required for axon pathfinding and extension in the C. elegans nerve ring." Development 126, no. 16 (August 15, 1999): 3679–92. http://dx.doi.org/10.1242/dev.126.16.3679.

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Over half of the neurons in Caenorhabditis elegans send axons to the nerve ring, a large neuropil in the head of the animal. Genetic screens in animals that express the green fluorescent protein in a subset of sensory neurons identified eight new sax genes that affect the morphology of nerve ring axons. sax-3/robo mutations disrupt axon guidance in the nerve ring, while sax-5, sax-9 and unc-44 disrupt both axon guidance and axon extension. Axon extension and guidance proceed normally in sax-1, sax-2, sax-6, sax-7 and sax-8 mutants, but these animals exhibit later defects in the maintenance of nerve ring structure. The functions of existing guidance genes in nerve ring development were also examined, revealing that SAX-3/Robo acts in parallel to the VAB-1/Eph receptor and the UNC-6/netrin, UNC-40/DCC guidance systems for ventral guidance of axons in the amphid commissure, a major route of axon entry into the nerve ring. In addition, SAX-3/Robo and the VAB-1/Eph receptor both function to prevent aberrant axon crossing at the ventral midline. Together, these genes define pathways required for axon growth, guidance and maintenance during nervous system development.
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Nishikimi, Mitsuaki, Koji Oishi, and Kazunori Nakajima. "Axon Guidance Mechanisms for Establishment of Callosal Connections." Neural Plasticity 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/149060.

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Numerous studies have investigated the formation of interhemispheric connections which are involved in high-ordered functions of the cerebral cortex in eutherian animals, including humans. The development of callosal axons, which transfer and integrate information between the right/left hemispheres and represent the most prominent commissural system, must be strictly regulated. From the beginning of their growth, until reaching their targets in the contralateral cortex, the callosal axons are guided mainly by two environmental cues: (1) the midline structures and (2) neighboring? axons. Recent studies have shown the importance of axona guidance by such cues and the underlying molecular mechanisms. In this paper, we review these guidance mechanisms during the development of the callosal neurons. Midline populations express and secrete guidance molecules, and “pioneer” axons as well as interactions between the medial and lateral axons are also involved in the axon pathfinding of the callosal neurons. Finally, we describe callosal dysgenesis in humans and mice, that results from a disruption of these navigational mechanisms.
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Stoeckli, Esther. "Where does axon guidance lead us?" F1000Research 6 (January 25, 2017): 78. http://dx.doi.org/10.12688/f1000research.10126.1.

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During neural circuit formation, axons need to navigate to their target cells in a complex, constantly changing environment. Although we most likely have identified most axon guidance cues and their receptors, we still cannot explain the molecular background of pathfinding for any subpopulation of axons. We lack mechanistic insight into the regulation of interactions between guidance receptors and their ligands. Recent developments in the field of axon guidance suggest that the regulation of surface expression of guidance receptors comprises transcriptional, translational, and post-translational mechanisms, such as trafficking of vesicles with specific cargos, protein-protein interactions, and specific proteolysis of guidance receptors. Not only axon guidance molecules but also the regulatory mechanisms that control their spatial and temporal expression are involved in synaptogenesis and synaptic plasticity. Therefore, it is not surprising that genes associated with axon guidance are frequently found in genetic and genomic studies of neurodevelopmental disorders.
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Liu, Zhi-Zhi, Jian Zhu, Chang-Ling Wang, Xin Wang, Ying-Ying Han, Ling-Yan Liu, and Hong A. Xu. "CRMP2 and CRMP4 Are Differentially Required for Axon Guidance and Growth in Zebrafish Retinal Neurons." Neural Plasticity 2018 (June 21, 2018): 1–9. http://dx.doi.org/10.1155/2018/8791304.

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Axons are directed to their correct targets by guidance cues during neurodevelopment. Many axon guidance cues have been discovered; however, much less known is about how the growth cones transduce the extracellular guidance cues to intracellular responses. Collapsin response mediator proteins (CRMPs) are a family of intracellular proteins that have been found to mediate growth cone behavior in vitro; however, their roles in vivo in axon development are much less explored. In zebrafish embryos, we find that CRMP2 and CRMP4 are expressed in the retinal ganglion cell layer when retinal axons are crossing the midline. Knocking down CRMP2 causes reduced elongation and premature termination of the retinal axons, while knocking down CRMP4 results in ipsilateral misprojections of retinal axons that would normally project to the contralateral brain. Furthermore, CRMP4 synchronizes with neuropilin 1 in retinal axon guidance, suggesting that CRMP4 might mediate the semaphorin/neuropilin signaling pathway. These results demonstrate that CRMP2 and CRMP4 function differentially in axon development in vivo.
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Shigeoka, Toshiaki, Bo Lu, and Christine E. Holt. "RNA-based mechanisms underlying axon guidance." Journal of Cell Biology 202, no. 7 (September 30, 2013): 991–99. http://dx.doi.org/10.1083/jcb.201305139.

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Axon guidance plays a key role in establishing neuronal circuitry. The motile tips of growing axons, the growth cones, navigate by responding directionally to guidance cues that pattern the embryonic neural pathways via receptor-mediated signaling. Evidence in vitro in the last decade supports the notion that RNA-based mechanisms contribute to cue-directed steering during axon guidance. Different cues trigger translation of distinct subsets of mRNAs and localized translation provides precise spatiotemporal control over the growth cone proteome in response to localized receptor activation. Recent evidence has now demonstrated a role for localized translational control in axon guidance decisions in vivo.
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Kellermeyer, Riley, Leah Heydman, Grant Mastick, and Thomas Kidd. "The Role of Apoptotic Signaling in Axon Guidance." Journal of Developmental Biology 6, no. 4 (October 18, 2018): 24. http://dx.doi.org/10.3390/jdb6040024.

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Navigating growth cones are exposed to multiple signals simultaneously and have to integrate competing cues into a coherent navigational response. Integration of guidance cues is traditionally thought to occur at the level of cytoskeletal dynamics. Drosophila studies indicate that cells exhibit a low level of continuous caspase protease activation, and that axon guidance cues can activate or suppress caspase activity. We base a model for axon guidance on these observations. By analogy with other systems in which caspase signaling has non-apoptotic functions, we propose that caspase signaling can either reinforce repulsion or negate attraction in response to external guidance cues by cleaving cytoskeletal proteins. Over the course of an entire trajectory, incorrectly navigating axons may pass the threshold for apoptosis and be eliminated, whereas axons making correct decisions will survive. These observations would also explain why neurotrophic factors can act as axon guidance cues and why axon guidance systems such as Slit/Robo signaling may act as tumor suppressors in cancer.
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Tuttle, R., J. E. Braisted, L. J. Richards, and D. D. O'Leary. "Retinal axon guidance by region-specific cues in diencephalon." Development 125, no. 5 (March 1, 1998): 791–801. http://dx.doi.org/10.1242/dev.125.5.791.

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Retinal axons show region-specific patterning along the dorsal-ventral axis of diencephalon: retinal axons grow in a compact bundle over hypothalamus, dramatically splay out over thalamus, and circumvent epithalamus as they continue toward the dorsal midbrain. In vitro, retinal axons are repulsed by substrate-bound and soluble activities in hypothalamus and epithalamus, but invade thalamus. The repulsion is mimicked by a soluble floor plate activity. Tenascin and neurocan, extracellular matrix molecules that inhibit retinal axon growth in vitro, are enriched in hypothalamus and epithalamus. Within thalamus, a stimulatory activity is specifically upregulated in target nuclei at the time that retinal axons invade them. These findings suggest that region-specific, axon repulsive and stimulatory activities control retinal axon patterning in the embryonic diencephalon.
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Bashaw, Greg J., Thomas Kidd, Dave Murray, Tony Pawson, and Corey S. Goodman. "Repulsive Axon Guidance." Cell 101, no. 7 (June 2000): 703–15. http://dx.doi.org/10.1016/s0092-8674(00)80883-1.

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Dissertations / Theses on the topic "Axon guidance"

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Ohler, Stephan. "Photoreceptor axon guidance in Drosophila melanogaster." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-144130.

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Goeke, Scott Charles. "The role of lola in axon guidance /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/10639.

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Lerner, Oleg. "Motor axon guidance to the extraocular muscles." Thesis, King's College London (University of London), 2006. https://kclpure.kcl.ac.uk/portal/en/theses/motor-axon-guidance-to-the-extraocular-muscles(4baaa0d2-474a-4b7e-86e5-dd434ac5a9f7).html.

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Zylbersztejn, Kathleen. "Role of vesicular traffic in axon guidance." Paris 7, 2011. http://www.theses.fr/2011PA077146.

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Lors du développement, les molécules de guidage attractives et répulsives, telles que les Sémaphorines (Sema), sont responsables de la formation du réseau neuronal des axones et des dendrites. Les molécules de guidage extracellulaire se lient à des récepteurs qui activent les voies de signalisation intracellulaire et remodèlent le cône de croissance. Le rôle du trafic membranaire dans le guidage axonale est encore largement inconnu. Le trafic membranaire nécessite les protéines SNARE pour la fusion membranaire. La SNARE vésiculaire Synaptobrévine2 (Syb2) est connue pour son rôle dans la libération des neurotransmetteurs dans les neurones matures tandis que TI-VAMP est principalement connue pour son rôle dans la croissance axonale. Leurs rôles potentiels dans le guidage axonale demeurent inconnus. J'ai montré que Syb2 est nécessaire pour la répulsion SemaSA-dépendante, mais pas pour l'attraction SemaSC-dépendante dans des neurones en culture et dans le cerveau murin. Syb2 interagit aussi avec Neuropilinel et PlexinAl, les deux éléments du récepteur à la SemaSA, via son domaine juxta-transmembranaire. Nous concluons que signalisation et la répulsion axonale SemaSA-dépendante nécessitent le trafic vésiculaire Syb2-dépendante. Nous proposons donc un modèle dans lequel la répulsion induite par la SemaSA requiert une endocytose locale accrue et une diminution de l'exocytose. La SemaSA est également impliquée dans le guidage de cellules non neuronales. Certaines de nos observations ont été obtenues dans des cellules non neuronales, suggérant que nos conclusions peuvent s'appliquer généralement à la signalisation de la SemaSA
During development, attractive and repulsive guidance molecules, such as semaphorins (Sema), are responsible for proper wiring of axons and dendrites. Attractive and repulsive external guidance cues bind to receptors which activate intracellular signalling pathways and reshape the growth cone. The role of vesicular traffic in axonal guidance is still largely unknown. Vesicular traffic requires SNAREs proteins for membrane fusion. The exocytic vesicular SNARE Synaptobrevin2 (Syb2) mediates neurotransmitter release in mature neurons while TI-VAMP is mainly known for mediating axon growth. Their potential roles in axon guidance remain elusive. According to a previous model, attraction would rely solely on Syb2-dependent exocytosis while repulsion would exclusively require endocytosis. However, my PhD work has hinted a more complex view on guidance mechanisms. I showed that Syb2 is required for SemaSA-dependent repulsion but not SemaSC-dependent attraction in cultured neurons and in the mouse brain. Syb2 associates with Neuropilinl and PlexinAl, two essential components of the SemaSA receptor, via its juxta-transmembrane domain. We concluded that SemaS A-mediated signalling and axonal repulsion require Syb2-dependent vesicular traffic. We thus propose a model in which SemaSA-induced repulsion is mediated by local increased endocytosis and decreased exocytosis. SemaSA is also involved in non neuronal cell navigation, Some of our observations were obtained in non-neuronal cells further suggesting that our conclusions may more generally apply to SemaSA signaling
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Eberhart, Johann. "EphA4/Ephrin interactions in motor axon guidance /." free to MU campus, to others for purchase, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060095.

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Suh, Christopher D. Y. "Identification of axon guidance molecules in C. elegans /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2006. http://uclibs.org/PID/11984.

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Yu, Li. "Dissection of Semaphorin reverse signaling in axon guidance." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96816.

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My PhD thesis describes original study in the guidance of photoreceptor (R-cell) axons in the developing Drosophila visual system. I investigate the role of the transmembrane protein Semaphorin1a (Sema1a) and PlexinA (PlexA) in R-cell axon guidance and dissect the Sema1a reverse signaling pathway. My results indicate that Sema1a functions as a receptor to mediate an attractive response in the Drosophila visual system, and PlexA acts as the upstream regulator of Sema1a.Semaphorins belong to a large family of both secreted and transmembrane proteins known as axon guidance molecules in vertebrates and invertebrates. Drosophila Sema1a is a transmembrane protein. Previous studies have shown that Sema1a functions as the ligand of its receptor PlexA together with Otk inducing a repulsive signaling pathway in the Drosophila neuromuscular system. However, whether it is the case in the Drosophila visual system remains unknown. Our results revealed that sema1a is required in R1-R6 axons for their association and guidance to form a proper topographic termination layer. The function of sema1a in R cells is cell-autonomous. Overexpression of sema1a causes a hyper-fasciculation phenotype in which abnormal thicker bundles are formed in both lamina and medulla. Interestingly, we found that the cytoplasmic domain of Sema1a is required for its function in R-cell axon guidance. All these results suggest that Sema1a functions as an attractive receptor to mediate R-cell interactions during R-cell axon projections, which is totally different with previous studies.Furthermore, I investigate the upstream ligand of Sema1a in our model by testing candidate-gene approach. I found that plexA displays a sema1a-like loss-of-function and gain-of-function phenotype in the Drosophila visual system. In addition, plexA genetically interacts with sema1a. These results indicate that plexA and sema1a function in the same signaling pathway. Interestingly, the cytoplasmic domain of PlexA is dispensable for its function in inducing the hyper-fasciculation phenotype in R-cell axon guidance, suggesting that PlexA functions as a ligand. Epistasis analysis suggests that plexA functions as an upstream regulator of sema1a. Taken all together, we propose that PlexA functions as the ligand of Sema1a in the Sema1a reverse signaling pathway in the Drosophila visual system.
Ma thèse de doctorat s'intéresse au rôle des protéines transmembranaires Semaphorin1a (Sema1a) et PlexinA (Plexa) au cours du guidage axonal des photorécepteurs ou cellules R dans le système visuel de la Drosophile. Mes résultats indiquent que Sema1a agit comme un récepteur contrôlant la transmission d'un signal attractif, tandis que PlexA agit en amont de Sema1a. Les sémaphorines sont des protéines soit sécrétées soit transmembranaires qui participent au guidage du cône axonal des neurones, à la régénération axonale, ainsi qu'au développement du tissu nerveux et d'autres tissus. Il a été démontré dans le système neuromusculaire de la Drosophile que Sema1a est une protéine transmembranaire qui, une fois liée a son récepteur PlexA, induit un signal répulsif. Notre analyse de mutants de perte-de-fonction Sema1a révèle que Sema1a est requise pour le guidage des cellules R1-6 et la mise en place de la topographie précise des terminaisons neuronales. La surexpression de Sema1a cause une hyper-fasciculation qui se traduit par la formation de faisceaux neuronaux anormalement épais dans la lamina et la medulla. De plus, nous avons trouvé que la portion cytoplasmique de Sema1a est requise pour son rôle dans le guidage des cellules R. Ainsi, mes résultats suggèrent un nouveau rôle pour Sema-1a en tant que récepteur modulant un effet attractif lors de la projection axonale. Qui plus est, par une approche de gènes candidats j'ai étudié les ligands en amont de Sema-1a. Cette analyse m'a permis de montrer que la perte de fonction ainsi que la surexpression de PlexA induisent des phénotypes similaires a ceux observés chez le mutant Sema1a ou lors de la surexpression de Sema-1a. J'ai également démontré que PlexA interagit génétiquement avec Sema-1a. Ces résultats démontrent que PlexA et Sema-1a fonctionnent au sein de la même voie de signalisation. De façon intéressante la queue cytoplasmique de PlexA est dispensable pour la formation des fascicules neuronaux suggérant que PlexA fonctionne comme un ligand. Finalement des études épistatiques suggèrent que PlexA est en amont de Sema-1a. En conclusion, nous proposons que dans le système visuel de la Drosophile, PlexA soit le ligand de Sema-1a dans une voie de signalisation Sema-1a inversée.
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Tayler, Timothy D. 1972. "Compartmentalization and axon guidance in the Drosophila brain." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/28937.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2005.
Includes bibliographical references.
The Drosophila brain is composed of many morphologically and functionally distinct processing centers and brain morphogenesis depends on the creation and maintenance of distinct boundaries between adjacent regions to prevent cells from mixing. In the Drosophila visual system, I have found that Slit and Roundabout (Robo) proteins function to prevent cells from adjacent compartments from mixing. I have defined a boundary between two distinct compartments, the lamina and lobula, and find that the secreted ligand Slit is present in the lamina, while the Robo receptors (Robo, Robo2 and Robo3) are expressed on lobula neurons. I examined the function of theses proteins by identifying a tissue-specific allele of slit and creating transgenic RNAi flies that inhibit the expression of the Robo proteins. Loss of Slit or all three Robo proteins in the visual system results in the invasion of lobula neurons into the lamina. Mixing of cells at the lamina/lobula boundary results in glial cell mispositioning and aberrant photoreceptor axon targeting. Thus, Slit and Robo proteins are required to restrict movement of cells across the lamina/lobula boundary. Additionally, I have characterized Ptpmeg, a highly conserved protein tyrosine phosphatase (PTP). In addition to the C-terminus PTP domain, Ptpmeg contains a central PDZ domain and an N-terminus FERM domain. The in vivo role of this family of proteins is unknown. To explore the function of Ptpmeg in flies, mutants were generated by targeted gene disruption. Examination of the adult nervous system of Ptpmeg mutants reveals a defect in the mushroom bodies (MB), brain structures required for olfactory learning and memory. In mutant animals, the MB lobes are disorganized and fail to elaborate their characteristic structure. I find
(cont.) that Ptpmeg is expressed on MB axons and targeted knockdown of Ptpmeg in the MB results in similar defects as seen in homozygous mutants. Thus, the MB neurons appear to require Ptpmeg for proper formation.
by Timothy D. Tayler.
Ph.D.
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Brown, Samantha. "The mechanisms controlling embryonic axon growth and guidance." Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=238413.

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My thesis investigated the mechanisms important for the development of the mammalian optic pathway and whether Primodos, a hormonal pregnancy test drug used between 1958 and 1978, has the potential to cause birth defects. I found that DSCAM (Down's syndrome cell adhesion molecule) is required for the fasciculation and growth of RGC axons. In mice carrying spontaneous mutations in DSCAM (Dscamdel17) normal axon pathfinding occurs. However, growth of axons from the optic chiasm towards their targets is impaired and axon organisation in the optic chiasm and tracts, and RGC growth cone morphologies, are also altered. Conversely, DSCAM gain-of-function resulted in exuberant growth into the dorsal thalamus. In vitro, DSCAM promotes RGC axon growth and fasciculation independently of cell contact. Along with previous work in the lab, my findings identified DSCAM as a permissive signal that promotes the growth and fasciculation of RGC axons. Spondins and their LRP binding partners are expressed in both the retina and around the developing optic pathway, consistent with a role in regulating growth of RGC axons towards visual targets. In vitro retinal explant cultures exposed to cells transfected with F-spondin, or its TSR domains, did not however provide evidence of axon growth modulation via F-spondin. I used Zebrafish embryos, a human cell-line and mouse retinal explants to investigate the actions of the components of Primodos upon embryonic axon growth, intersomitic vessel development and changes to cell number, proliferation and cell death. NA/EE-mixture exposure caused rapid morphological damage in Zebrafish embryos, affecting multiple organ systems and affecting physical movement. The NA/EE-mixture also affects nerve outgrowth and blood vessel patterning directly and accumulates in the III developing embryo for at least 24 hours. These data demonstrate that Norethisterone acetate and Ethinyl estradiol are potentially teratogenic, depending on dose applied and embryonic stage of development.
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Sun, Qi Zinn Kai George. "Molecular genetics of axon guidance in Drosophila melanogaster /." Diss., Pasadena, Calif. : California Institute of Technology, 2000. http://resolver.caltech.edu/CaltechETD:etd-03242005-130557.

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Books on the topic "Axon guidance"

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Bagnard, Dominique, ed. Axon Growth and Guidance. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-76715-4.

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Dominique, Bagnard, ed. Axon growth and guidance. New York: Springer Science + Business Media, 2007.

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Binns, Kathleen Leslie. Phosphopeptide mapping of axon guidance molecules by Nano-ESI tandem mass spectrometry. Ottawa: National Library of Canada, 2002.

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Murray, David Andrew. The binding of proteins with modular domains to the cytoplasmic domain of the axon guidance receptor human roundaboutl. Ottawa: National Library of Canada, 2001.

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Poo, Mu-Ming, and Joshua Sanes. Abstracts of papers presented at the 2004 meeting on axon guidance & neural plasticity: September 18-September 22, 2004. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2004.

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Poo, Mu-Ming. Abstracts of papers presented at the 2006 meeting on axon guidance, synaptogenesis & neural plasticity: Sept. 13-Sept. 17, 2006. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2006.

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Kolodkin, Alex. Abstracts of papers presented at the 2006 meeting on axon guidance, synaptogenesis & neural plasticity: Sept. 10-Sept. 14, 2008. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2006.

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Steven, Robert Michael. The molecular cloning and characterization of unc-73: A complex gene that plays a role in axon guidance and cell migration in Caenorhabditis elegans. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1998.

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Bagnard, Dominique Ph D. Axon Growth And Guidance. Landes Bioscience, 2006.

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Bagnard, Dominique, and Various. Axon Growth and Guidance. Springer, 2010.

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Book chapters on the topic "Axon guidance"

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Tannahill, David, Geoff M. W. Cook, and Roger J. Keynes. "Axon guidance and somites." In Molecular Bases of Axonal Growth and Pathfinding, 275–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60905-3_13.

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Blockus, Heike, and Alain Chédotal. "Disorders of Axon Guidance." In The Genetics of Neurodevelopmental Disorders, 155–94. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118524947.ch8.

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Imai, Fumiyasu, and Yutaka Yoshida. "Axon Guidance in the Spinal Cord." In Semaphorins, 39–63. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-54385-5_3.

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Stoeckli, Esther T., and Vera Niederkofler. "Molecular Aspects of Commissural Axon Guidance." In New Aspects of Axonal Structure and Function, 3–18. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1676-1_1.

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Prasad, Asheeta A., and R. Jeroen Pasterkamp. "Axon Guidance in the Dopamine System." In Advances in Experimental Medicine and Biology, 91–100. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0322-8_9.

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Chédotal, Alain. "Chemotropic Axon Guidance Molecules in Tumorigenesis." In Neuronal Activity in Tumor Tissue, 78–90. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000100048.

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Piper, Michael, Francis van Horck, and Christine Holt. "The Role of Cyclic Nucleotides in Axon Guidance." In Advances in Experimental Medicine and Biology, 134–43. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-76715-4_10.

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Luck, Robert, and Carmen Ruiz de Almodovar. "Axon Guidance Factors in Developmental and Pathological Angiogenesis." In Endothelial Signaling in Development and Disease, 259–91. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2907-8_11.

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de Wit, Joris, and Joost Verhaagen. "Proteoglycans as Modulators of Axon Guidance Cue Function." In Advances in Experimental Medicine and Biology, 73–89. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-70956-7_7.

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Robichaux, Michael A., and Christopher W. Cowan. "Signaling Mechanisms of Axon Guidance and Early Synaptogenesis." In The Neurobiology of Childhood, 19–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-662-45758-0_255.

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Conference papers on the topic "Axon guidance"

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Aletti, Giacomo, Paola Causin, Giovanni Naldi, Luigi M. Ricciardi, Aniello Buonocore, and Enrica Pirozzi. "A Model for Axon Guidance: Sensing, Transduction and Movement." In COLLECTIVE DYNAMICS: TOPICS ON COMPETITION AND COOPERATION IN THE BIOSCIENCES: A Selection of Papers in the Proceedings of the BIOCOMP2007 International Conference. AIP, 2008. http://dx.doi.org/10.1063/1.2965082.

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Siriwardane, M. L., K. E. DeRosa, and B. J. Pfister. "Collagen-based fiber-gel constructs engineered for schwann cell guidance and adult axon growth." In 2011 37th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2011. http://dx.doi.org/10.1109/nebc.2011.5778694.

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Yong, Lin-Kin, Dali Li, Ethan Poteet, Zhengdong Liang, William Fisher, Changyi Chen, and Qizhi Cathy Yao. "Abstract 3574: Novel roles of an axon-guidance molecule, semaphorin 3E, in pancreatic cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3574.

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Biankin, Andrew V., John D. McPherson, and Richard A. Gibbs. "Abstract IA3: Genomic analysis reveals roles for chromatin modification and axon guidance in pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-ia3.

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Biankin, Andrew V., John D. McPherson, Richard A. Gibbs, and Sean M. Grimmond. "Abstract LB-404: Genomic analysis reveals roles for chromatin modification and axon guidance in pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-404.

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Turpin, Anthony, Carine Delliaux, Tian Tian, Nathalie Vanpouille, Anne Flourens, Rachel Deplus, Xavier Leroy, Yvan de Launoit, and Martine Duterque-Coquillaud. "Abstract 694: Axon guidance neuropilin and plexin A2 genes are involved in ERG-associated prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-694.

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Cai, Shurui, Renata Fu, Kevin Wang, Na Li, Haowen Chen, Ellie Xi, Daniel Lin, Yongsheng Bai, and Qi-En Wang. "Bioinformatics analysis of miRNAs identifies enrichment of axon guidance pathway genes in ovarian cancer stem cells." In 2021 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2021. http://dx.doi.org/10.1109/bibm52615.2021.9669299.

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Bhattacharjee, N., N. Li, and A. Folch. "A neuron-benign microfluidic gradient generator for studying the growth of mammalian neurons towards axon guidance factors." In TRANSDUCERS 2009 - 2009 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2009. http://dx.doi.org/10.1109/sensor.2009.5285619.

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Elhassan, Mohamed O., Jennifer Christie, Marlieke Molendijk, and Mark Duxbury. "Abstract 5272: Multimodality interrogation of systemic RNA interference-defective-1 transmembrane family member 1 (SIDT1) identifies axon guidance protein interactions." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5272.

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Körner, S., N. Thau-Habermann, and S. Petri. "Die Expression des Axon-guidance Protein Rezeptor Neuropilin 1 ist im Rückenmark von transgenen SOD1G93A ALS Mäusen erhöht und im Muskel erniedrigt." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685003.

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Reports on the topic "Axon guidance"

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Selleck, Scott B. Understanding the Function of Tuberous Sclerosis Complex Genes in Neural Development: Roles in Synapse Assembly and Axon Guidance. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada603854.

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