共 39 条
Transforming JAK1 mutations exhibit differential signalling, FERM domain requirements and growth responses to interferon-γ
被引:20
作者:

Gordon, Geoff M.
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H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA
Univ S Florida, Canc Biol PhD Program, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA

Lambert, Que T.
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机构:
H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA

Daniel, Kenyon G.
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机构: H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA

Reuther, Gary W.
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机构:
H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA
机构:
[1] H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA
[2] Univ S Florida, Canc Biol PhD Program, Tampa, FL 33612 USA
关键词:
acute leukaemia;
4.1/ezrin/radixin/moesin (FERM) domain;
interferon-gamma;
Janus kinase 1 (JAK1);
transformation;
tyrosine kinase;
ACUTE LYMPHOBLASTIC-LEUKEMIA;
TYROSINE KINASE JAK2;
JANUS KINASES;
POLYCYTHEMIA-VERA;
CYTOKINE RECEPTOR;
MYELOPROLIFERATIVE DISORDERS;
CONSTITUTIVE ACTIVATION;
PSEUDOKINASE DOMAIN;
IDENTIFICATION;
SPECIFICITY;
D O I:
10.1042/BJ20100774
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Recent work has highlighted roles for JAK (Janus kinase) family members in haemopoietic diseases. Although sequencing efforts have uncovered transforming JAK1 mutations in acute leukaemia, they have also identified non-transforming JAM mutations. Thus with limited knowledge of the mechanisms of JAK1 activation by mutation, sequencing may not readily identify transforming mutations. Therefore we sought to further understand the repertoire of transforming mutations of JAK1. We identified seven randomly generated transforming JAK mutations, including V658L and a deletion of amino acids 629-630 in the pseudokinase domain, as well as L9 10P, F938S, P960S, K1026E and Y1035C within the kinase domain. These mutations led to differential signalling activation, but exhibited similar transforming abilities, in BaF3 cells. Interestingly, these properties did not always correlate with JAK1 activation-loop phosphorylation. We also identified a JAK1 mutant that did not require a functional FERM (4.1/ezrin/radixin/moesin) domain for transformation. Although we isolated a mutation of JAK1 at residue Val(658), which is found mutated in acute leukaemia patients, most of the mutations we identified are within the kinase domain and have yet to be identified in patients. Interestingly, compared with cells expressing JAK1-V658F, cells expressing these mutants had higher STAT1 (signal transducer and activator of transcription 1) phosphorylation and were more sensitive to interferon-gamma-mediated growth inhibition. The differential STAT1 activation and interferon-sensitivity of JAK1 mutants may contribute to the determination of which specific JAK1 mutations ultimately contribute to disease and thus are identified in patients. Our characterization of these novel mutations contributes to a better understanding of mutational activation of JAK1.
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页码:255 / 265
页数:11
相关论文
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Haan, Serge
论文数: 0 引用数: 0
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg
Uniklin Aachen, Inst Biochem, D-5100 Aachen, Germany Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Margue, Christiane
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Engrand, Arnaud
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Rolvering, Catherine
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

de Leur, Hildegard Schmitz-Van
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Uniklin Aachen, Inst Biochem, D-5100 Aachen, Germany Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Heinrich, Peter C.
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Uniklin Aachen, Inst Biochem, D-5100 Aachen, Germany Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Behrmann, Iris
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg

Haan, Claude
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Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg Univ Luxembourg, Fac Sci Technol & Commun, Life Sci Res Unit, L-1511 Luxembourg, Luxembourg
[10]
The mutation in the ATP-binding region of JAK1, identified in human uterine leiomyosarcomas, results in defective interferon-γ inducibility of TAP1 and LMP2
[J].
Hayashi, T.
;
Kobayashi, Y.
;
Kohsaka, S.
;
Sano, K.
.
ONCOGENE,
2006, 25 (29)
:4016-4026

Hayashi, T.
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机构: Shinshu Univ, Sch Med, Dept Immunol & Infect Dis, Nagano 3908621, Japan

Kobayashi, Y.
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机构: Shinshu Univ, Sch Med, Dept Immunol & Infect Dis, Nagano 3908621, Japan

Kohsaka, S.
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机构: Shinshu Univ, Sch Med, Dept Immunol & Infect Dis, Nagano 3908621, Japan

Sano, K.
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机构: Shinshu Univ, Sch Med, Dept Immunol & Infect Dis, Nagano 3908621, Japan