Normal and oncogenic forms of the receptor tyrosine kinase kit

被引:233
作者
Lennartsson, J [1 ]
Jelacic, T [1 ]
Linnekin, D [1 ]
Shivakrupa, R [1 ]
机构
[1] NCI, Basic Res Lab, Canc Res Ctr, Frederick, MD 21701 USA
关键词
kit; signal transduction; hematopoiesis; oncogene; cancer;
D O I
10.1634/stemcells.2004-0117
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Kit is a receptor tyrosine kinase (RTK) that binds stem cell factor. This receptor ligand combination is important for normal hematopoiesis, as well as pigmentation, gut function, and reproduction. Structurally, Kit has both an extracellular and intracellular region. The intracellular region is comprised of a juxtamembrane domain (JMD), a kinase domain, a kinase insert, and a carboxyl tail. Inappropriate expression or activation of Kit is associated with a variety of diseases in humans. Activating mutations in Kit have been identified primarily in the JMD and the second part of the kinase domain and have been associated with gastrointestinal stromal cell tumors and mastocytosis, respectively. There are also reports of activating mutations in some forms of germ cell tumors and core binding factor leukemias. Since the cloning of the Kit ligand in the early 1990s, there has been an explosion of information relating to the mechanism of action of normal forms of Kit as well as activated mutants. This is important because understanding this RTK at the biochemical level could assist in the development of therapeutics to treat primary and secondary defects in the tissues that require Kit. Furthermore, understanding the mechanisms mediating transformation of cells by activated Kit mutants will help in the design of interventions for human disease associated with these mutations. The objective of this review is to summarize what is known about normal and oncogenic forms of Kit. We will place particular emphasis on recent developments in understanding the mechanisms of action of normal and activated forms of this RTK and its association with human disease, particularly in hematopoietic cells.
引用
收藏
页码:16 / 43
页数:28
相关论文
共 269 条
[71]   ACTIVATION OF RAS IN-VITRO AND IN INTACT FIBROBLASTS BY THE VAV GUANINE-NUCLEOTIDE EXCHANGE PROTEIN [J].
GULBINS, E ;
COGGESHALL, KM ;
LANGLET, C ;
BAIER, G ;
BONNEFOYBERARD, N ;
BURN, P ;
WITTINGHOFER, A ;
KATZAV, S ;
ALTMAN, A .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (02) :906-913
[72]  
GUTMAN M, 1994, ANTICANCER RES, V14, P1759
[73]   GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AND STEEL FACTOR INDUCE PHOSPHORYLATION OF BOTH UNIQUE AND OVERLAPPING SIGNAL TRANSDUCTION INTERMEDIATES IN A HUMAN FACTOR-DEPENDENT HEMATOPOIETIC-CELL LINE [J].
HALLEK, M ;
DRUKER, B ;
LEPISTO, EM ;
WOOD, KW ;
ERNST, TJ ;
GRIFFIN, JD .
JOURNAL OF CELLULAR PHYSIOLOGY, 1992, 153 (01) :176-186
[74]  
Hart SM, 2002, HAEMATOLOGICA, V87, P1307
[75]   Necessity of tyrosine 719 and phosphatidylinositol 3′-kinase-mediated signal pathway in constitutive activation and oncogenic potential of c-kit receptor tyrosine kinase with the Asp814Val mutation [J].
Hashimoto, K ;
Matsumura, I ;
Tsujimura, T ;
Kim, DK ;
Ogihara, H ;
Ikeda, H ;
Ueda, S ;
Mizuki, M ;
Sugahara, H ;
Shibayama, H ;
Kitamura, Y ;
Kanakura, Y .
BLOOD, 2003, 101 (03) :1094-1102
[76]  
Hashimoto K, 1996, AM J PATHOL, V148, P189
[77]   Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor [J].
Heinrich, MC ;
Griffith, DJ ;
Druker, BJ ;
Wait, CL ;
Ott, KA ;
Zigler, AJ .
BLOOD, 2000, 96 (03) :925-932
[78]   Inhibition of KIT tyrosine kinase activity: A novel molecular approach to the treatment of KIT-positive malignancies [J].
Heinrich, MC ;
Blanke, CD ;
Druker, BJ ;
Corless, CL .
JOURNAL OF CLINICAL ONCOLOGY, 2002, 20 (06) :1692-1703
[79]   PDGFRA activating mutations in gastrointestinal stromal tumors [J].
Heinrich, MC ;
Corless, CL ;
Duensing, A ;
McGreevey, L ;
Chen, CJ ;
Joseph, N ;
Singer, S ;
Griffith, DJ ;
Haley, A ;
Town, A ;
Demetri, GD ;
Fletcher, CDM ;
Fletcher, JA .
SCIENCE, 2003, 299 (5607) :708-710
[80]   Recruitment of stem and progenitor cells from the bone marrow niche requires MMP-9 mediated release of Kit-ligand [J].
Heissig, B ;
Hattori, K ;
Dias, S ;
Friedrich, M ;
Ferris, B ;
Hackett, NR ;
Crystal, RG ;
Besmer, P ;
Lyden, D ;
Moore, MAS ;
Werb, Z ;
Rafii, S .
CELL, 2002, 109 (05) :625-637