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Table of Contents
Vol. 106, No. 4, 1995
Issue release date: 1995
Section title: Original Paper
Int Arch Allergy Immunol 1995;106:377–385
(DOI:10.1159/000236870)

Substitution of an Aspartic Acid Results in Constitutive Activation of c-kitReceptor Tyrosine Kinase in a Rat Tumor Mast Cell Line RBL-2H3

Tsujimura T.a · Furitsu T.b · Morimoto M.a · Kanayama Y.b · Nomura S.a · Matsuzawa Y.b · Kitamura Y.a · Kanakura Y.b
Departments of aPathology, and bInternal Medicine II, Osaka University, Medical School, Suita, Osaka, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: July 12, 1994
Accepted: December 06, 1994
Published online: September 04, 2009
Issue release date: 1995

Number of Print Pages: 9
Number of Figures: 0
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA

Abstract

The c-kit protooncogene encodes a receptor tyrosine kinase that mediates signals required for differentiation, proliferation and survival of mast cells. We have already shown the constitutive activation of c-kit receptor tyrosine kinase (KIT) in a human mast cell leukemia line (HMC-1) and a murine mastocytoma cell line (P-815). We here examined whether such constitutive activation of KIT occurred in the rat tumor mast cell line RBL-2H3 as well, which is frequently used as a tool for studying functions of mast cells. In RBL-2H3 cells, KIT was constitutively phosphorylated on tyrosine and activated in the absence of autocrine production of its ligand, stem cell factor (SCF). Sequencing analysis revealed that one of c-kit genes of RBL-2H3 cells had a point mutation, resulting in amino acid substitution of Tyr for Asp in codon 817. When rat wild-type c-kit cDNA and mutant-type c-kit cDNA encoding KITTyr817 were transfected into cells of a human embryonic kidney cell line (293T), only mutant form KITTyr817 was constitutively phosphorylated on tyrosine and activated in the absence of SCF. Since mutations at the same Asp codon constitutively activated KIT in all the human HMC-1, murine P-815, and rat RBL-2H3 cell lines, and since the incorporation of anti-sense oligonucleotides of c-kit messenger RNA significantly suppressed the proliferation of RBL-2H3 cells, the activating mutations in the Asp codon of the c-kit gene appeared to be involved in neoplastic growth of mast cells.

© 1995 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: July 12, 1994
Accepted: December 06, 1994
Published online: September 04, 2009
Issue release date: 1995

Number of Print Pages: 9
Number of Figures: 0
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA


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