Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-3-1
pubmed:abstractText
We investigated the roles of netrin-1 and slit-2 in regulation and navigation of dopamine (DA) axon growth using an explant culture preparation of embryonic ventral midbrain (embryonic day 14) and a co-culture system. We found that netrin-1 protein significantly enhanced DA axonal outgrowth and promoted DA axonal outgrowth in a co-culture system of netrin-1 expressing cells. Such effects were mediated by the receptor DCC as demonstrated by antibody perturbation of the DCC receptor. In contrast, slit-2 inhibited DA neuron extensions and repelled DA neurite growth. These slit-2 activities required robo receptors since the reduced neurite extension was abolished by addition of excess robo receptors. In this system, netrin-1 stimulated and slit-2 opposed DA neurite growth. Such regulation may be important for DA axonal maintenance, regeneration, and phenotypic target recognition.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules, http://linkedlifedata.com/resource/pubmed/chemical/DCC protein, human, http://linkedlifedata.com/resource/pubmed/chemical/G Protein-Coupled..., http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances, http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides..., http://linkedlifedata.com/resource/pubmed/chemical/Nerve Growth Factors, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Inwardly..., http://linkedlifedata.com/resource/pubmed/chemical/ROBO2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Slit homolog 2 protein, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine 3-Monooxygenase, http://linkedlifedata.com/resource/pubmed/chemical/netrin-1
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1044-7431
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
547-55
pubmed:dateRevised
2009-10-1
pubmed:meshHeading
pubmed-meshheading:15737744-Animals, pubmed-meshheading:15737744-Cell Adhesion Molecules, pubmed-meshheading:15737744-Cell Differentiation, pubmed-meshheading:15737744-Cell Line, pubmed-meshheading:15737744-Cells, Cultured, pubmed-meshheading:15737744-Dopamine, pubmed-meshheading:15737744-G Protein-Coupled Inwardly-Rectifying Potassium Channels, pubmed-meshheading:15737744-Growth Cones, pubmed-meshheading:15737744-Growth Inhibitors, pubmed-meshheading:15737744-Growth Substances, pubmed-meshheading:15737744-Humans, pubmed-meshheading:15737744-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:15737744-Mesencephalon, pubmed-meshheading:15737744-Nerve Growth Factors, pubmed-meshheading:15737744-Nerve Tissue Proteins, pubmed-meshheading:15737744-Neurites, pubmed-meshheading:15737744-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:15737744-Rats, pubmed-meshheading:15737744-Rats, Sprague-Dawley, pubmed-meshheading:15737744-Receptors, Cell Surface, pubmed-meshheading:15737744-Receptors, Immunologic, pubmed-meshheading:15737744-Substantia Nigra, pubmed-meshheading:15737744-Tumor Suppressor Proteins, pubmed-meshheading:15737744-Tyrosine 3-Monooxygenase
pubmed:year
2005
pubmed:articleTitle
Netrin-1 and slit-2 regulate and direct neurite growth of ventral midbrain dopaminergic neurons.
pubmed:affiliation
Neuroregeneration Laboratories, Mailman Research Center, Harvard Medical School/McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA. llin@mclean.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural