Linked Life Data

1922361

Source:http://linkedlifedata.com/resource/pubmed/id/1922361

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6344
pubmed:dateCreated
1991-11-7
pubmed:databankReference
pubmed:abstractText
Kallmann's syndrome (clinically characterized by hypogonadotropic hypogonadism and inability to smell) is caused by a defect in the migration of olfactory neurons, and neurons producing hypothalamic gonadotropin-releasing hormone. A gene has now been isolated from the critical region on Xp22.3 to which the syndrome locus has been assigned: this gene escapes X inactivation, has a homologue on the Y chromosome, and shows an unusual pattern of conservation across species. The predicted protein has significant similarities with proteins involved in neural cell adhesion and axonal pathfinding, as well as with protein kinases and phosphatases, which suggests that this gene could have a specific role in neuronal migration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
353
pubmed:geneSymbol
KALIG-1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
529-36
pubmed:dateRevised
2010-10-4
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
A gene deleted in Kallmann's syndrome shares homology with neural cell adhesion and axonal path-finding molecules.
pubmed:affiliation
Institute for Molecular Genetics, Baylor College of Medicine, Houston, Texas 77030.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't