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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1997-8-7
pubmed:abstractText
We investigated the mechanism of constitutive activation of c-kit receptor tyrosine kinase (KIT) found in the FMA3 murine mastocytoma cell line, and compared it with the mechanisms observed in other tumor mast cell lines (the HMC-1 human mast cell leukemia cell line, the RBL-2H3 rat mast cell leukemia cell line, and the P-815 murine mastocytoma cell line). The c-kit gene obtained from FMA3 cells was found to have 21-base deletion at the juxtamembrane domain of KIT, thereby leading to the constitutive activation of KIT. The deletion at the juxtamembrane domain resulted in constitutive dimerization of c-kit proteins, whereas the point mutation that were detected at the kinase domain of KIT in HMC-1, RBL-2H3, and P-815 cells caused constitutive activation of KIT without dimerization. These constitutively activating mutations of c-kit may play a role in development of mast cell tumors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0887-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
11 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
396-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Mechanisms of constitutive activation of c-kit receptor tyrosine kinase.
pubmed:affiliation
Department of Pathology, Osaka University Medical School, Suita, Japan.
pubmed:publicationType
Journal Article, Comparative Study