Linked Life Data

21339639

Source:http://linkedlifedata.com/resource/pubmed/id/21339639

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-3-2
pubmed:abstractText
Mutations in GLI3, a component of the Sonic Hedgehog (Shh) signaling pathway, cause a variety of human developmental syndromes. In this issue of the JCI, Cain and colleagues show that tightly regulated GLI3 repressor activity is essential for Shh-dependent differentiation of upper urinary tract pacemaker cells and the efficient flow of urine from the kidney to the bladder. These results link defective pacemaker cell differentiation with hydronephrosis and provide a cellular basis for one of the abnormal renal defects observed in humans with the GLI3-linked disease Pallister-Hall syndrome.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1558-8238
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
121
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
836-8
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Upper urinary tract pacemaker cells join the GLI club.
pubmed:affiliation
Department of Physiology and Biophysics, Cornell University Medical College, New York, New York 10021-4805, USA. daherzli@med.cornell.edu
pubmed:publicationType
Journal Article, Comment, Research Support, N.I.H., Extramural