Linked Life Data

7682073

Source:http://linkedlifedata.com/resource/pubmed/id/7682073

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-5-3
pubmed:databankReference
pubmed:abstractText
The c-kit protooncogene encodes a tyrosine kinase receptor expressed during ontogeny and adult life by several important and developmentally distinct cell lineages. Mice carrying germ line c-kit mutations exhibit deficiencies in most of these lineages, demonstrating that c-kit function is necessary for their normal development. To facilitate the identification of cis-acting elements which regulate tissue-specific c-kit expression, we cloned and characterized a mouse c-kit promoter which is functional in different cell types. A major c-kit transcription initiation site (TIS), located 58 bp upstream from the translation initiation codon, is utilized in mouse mast cells and in c-kit-positive cells in the mouse cerebellum. The effects of deletions in the 5' flanking region on reporter gene activity identify three short regulatory regions which function in both mouse and human c-kit positive cell lines. The nucleotide sequence of this region does not include CCAAT or TATA boxes but contains consensus binding sites for Sp1, Ap-2 and several short GA-rich elements which resemble binding sites for the ETS-domain proteins.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
191
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
893-901
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Cloning and functional analysis of the mouse c-kit promoter.
pubmed:affiliation
Department of Pathology, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't